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1
Davis-Harrison, Rebecca L., Narjes Tavoosi, Mary Clay, John M. Boettcher, Chad M. Rienstra, and James H. Morrissey. "Structural Insights Into How Clotting Proteins with GLA Domains Bind to Membrane Surfaces." Blood 116, no. 21 (November 19, 2010): 1141. http://dx.doi.org/10.1182/blood.v116.21.1141.1141.
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Abstract Abstract 1141 Most steps in the blood coagulation cascade obligatorily take place on membrane surfaces and are dependent on the exposure of phosphatidylserine (PS). Many coagulation proteins bind to PS-containing membrane bilayers in a calcium-dependent manner via gamma-carboxyglutamate-rich (GLA) domains. In spite of their importance, a clear picture of how GLA domains bind to the membrane interface has yet to emerge. A further intriguing aspect of the membrane's role in blood coagulation is that certain phospholipids, most notably phosphatidylethanolamine (PE), strongly synergize with PS to promote clotting reactions. The mechanisms of this synergy, and of PE's contribution to GLA domain binding, are poorly understood – although a number of hypotheses have been put forward. We now propose a new hypothesis to explain GLA domain binding to membranes, which we term the ABC (Anything But Choline) hypothesis; it invokes two main types of protein-phospholipid interactions: a single L-serine-specific binding site in each GLA domain; and multiple “phosphate-specific” interactions in which the phosphate groups of non-phosphatidylcholine phospholipids form coordination complexes with the tightly bound calcium ions in GLA domains. We have utilized liposomes and nanoscale phospholipid bilayers (Nanodiscs) in studies employing a series of techniques including solid-state NMR (SSNMR) and surface plasmon resonance (SPR) to address the mechanism of GLA domain-membrane interactions. We provide direct evidence in favor of the ABC hypothesis for GLA domain binding to membrane surfaces. Using SSNMR, we demonstrate that two distinct PS headgroup conformations are induced by binding of calcium ions, and that a third, novel PS headgroup conformation is induced when the prothrombin GLA domain engages the membrane. SPR studies have allowed for the determination of thermodynamic profiles of GLA domains interacting with phospholipid bilayers containing PS and/or PE, providing further insights to the mechanisms of GLA domain-membrane interactions. Disclosures: No relevant conflicts of interest to declare.
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Rabkin, Simon W. "Endothelin but Not Angiotensin II May Mediate Hypertension-Induced Coronary Vascular Calcification in Chronic Kidney Disease." International Journal of Nephrology 2011 (2011): 1–7. http://dx.doi.org/10.4061/2011/516237.
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To understand the relationship between putative neurohormonal factors operative in hypertension and coronary artery calcification (CAC), the relevant cellular actions of angiotensin (Ang II) and endothelin-1 (ET-1) are reviewed. There is compelling evidence to implicate ET-1 in CAC. ET-1 increases phosphate transport with a 42 to 73% increase inVmax. Increased cellular phosphate may induce CAC through increased Ca x phosphate product, transformation of vascular smooth muscle cells into a bone-producing phenotype or cell apoptosis that releases procalcific substances. ET-1 is increased in several models of vascular calcification. ET-1 inhibits inhibitors of calcification, matrix Gla and osteoprotegerin, while enhancing pro-calcific factors such as BMP-2 and osteopontin. In contrast, Ang II inhibits phosphate transport decreasingVmaxby 38% and increases matrix Gla. Ang II also stimulates bone resorption. Vascular calcification is reduced by ET-1 A receptor antagonists and to a greater extent than angiotensin receptor blockade although both agents reduce blood pressure.
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Frustaci, Andrea, Behzad Najafian, Giuseppe Donato, Romina Verardo, Cristina Chimenti, Luigi Sansone, Manuel Belli, Enza Vernucci, and Matteo Antonio Russo. "Divergent Impact of Enzyme Replacement Therapy on Human Cardiomyocytes and Enterocytes Affected by Fabry Disease: Correlation with Mannose-6-phosphate Receptor Expression." Journal of Clinical Medicine 11, no. 5 (February 28, 2022): 1344. http://dx.doi.org/10.3390/jcm11051344.
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Background: The impact of enzyme replacement therapy (ERT) on cardiomyocytes and intestinal cells, affected by Fabry disease (FD), is still unclear. Methods: Six patients with FD, including five family members with GLA mutation c.666delC and one with GLA mutation c.658C > T, manifesting cardiomyopathy and intestinal symptoms (abdominal pain, diarrhea and malabsorption) were included in the study. Clinical outcome, cardiac magnetic resonance (CMR), endomyocardial and gastro-intestinal biopsies were evaluated before and after 2 years of treatment with agalsidase-α (0.2 mg/kg every other week). Immunohistochemistry and Western blot assessments of mannose-6-phosphate receptors (IGF-II-R) on intestinal and myocardial frozen tissue were obtained at diagnosis and after 2 years of ERT. Results: After ERT left ventricular maximal wall thickness, ranging from pre (<10.5 mm) to mild (<15 mm) and moderate hypertrophy (16 mm), was not associated with significant changes at CMR. Degree of dyspnea, mean cardiomyocyte diameter and % vacuolated areas of cardiomyocytes, representing intracellular GL3, remained unmodified. In contrast, intestinal symptoms improved with disappearance of diarrhea, recovery of anemia and weight gain, correlating with near complete clearance of the enterocytes from GL3 inclusions. IGF-II-R expression was remarkably higher even at histochemistry in intestinal tissue compared with myocardium (p < 0.001) either at baseline and after ERT, thus justifying intestinal recovery. Conclusions: Human cells affected by FD may respond differently to ERT: while cardiomyocytes retain their GL3 content after 2 years of treatment, gastro-intestinal cells show GL3 removal with recovery of function. This divergent response may be related to differences in cellular turnover, as well as tissue IGF-II-R expression.
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Madjid, Armeida Dwi Ridhowati, Merpiseldin Nitsae, and Akhmad Sabarudin. "Perbandingan Butiran Kitosan dengan Pengikat Silang Epiklorohidrin (ECH) dan Glutaraldehid (GLA): Karakterisasi dan Kemampuan Adsorpsi Timbal (Pb)." ALCHEMY 6, no. 1 (March 30, 2018): 29. http://dx.doi.org/10.18860/al.v6i1.6790.
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<table width="661" border="1" cellspacing="0" cellpadding="0"><tbody><tr><td valign="top" width="408"><p class="BodyAbstract">Chitosan was an abundantly available source but it has a drawback which unstable in acid or base. So, it must be added with a crosslinker. In this article, we would compare the using of 2 crosslinkers, glutaraldehyde (GLA) and epichlorohydrin (ECH). Chitosan was formed as bead using tripolyphosphate (TPP). Chitosan beads crosslinked with GLA became browny beads and chitosan beads crosslinked with ECH became pearly white. IR characterization showed peaks in 1640 and 1540 cm<sup>-1</sup> represent phosphate contained TPP. There is no significant or unique peak differ GLA chitosan bead from ECH chitosan bead. Adsorption capacity of lead (Pb) in ECH chitosan bead was higher than in GLA chitosan bead. Morphology in SEM characterization exhibited a crinkle GLA chitosan bead then ECH chitosan bead.</p><p class="BodyAbstract"> </p><p class="BodyAbstract">Kitosan merupakan polimer alam dengan ketersediaan yang meruah tetapi memiliki kelemahan yaitu kurang stabil dalam asam maupun basa sehingga diperlukan pengikat silang. Dalam artikel ini akan dibandingkan dengan penggunaan 2 agen pengikatsilang yang dapat mengatasi permasalahan tersebut yaitu epiklorohidrin (ECH) dan glutaraldehid (GLA). Untuk pembuatan butiran kitosan digunakan tripolyphosphate (TPP). Setelah menjadi butiran kitosan diikatsilangkan dengan GLA menjadi butiran kitosan yang berwarna kecoklatan dan diikatsilangkan dengan ECH menjadi butiran kitosan bening. Karakterisasi spektrofotometri Infra Merah menunjukkan puncak pada daerah 1640 dan 1540 cm<sup>-1</sup> yang merupakan serapan khas dari tripolyphospate sedangkan tidak nampak perbedaan puncak spektra yang signifikan dari butiran kitosan GLA maupun ECH. Kemampuan adsorpsi butiran logam timbal (Pb) butiran kitosan ECH lebih tinggi jika dibandingkan dengan butiran kitosan GLA. Morfologi butiran kitosan dianalisis menggunakan Scanning Electron Morphology (SEM) dan menunjukkan bahwa morfologi untuk butiran GLA memiliki morfologi yang lebih berkerut jika dibandingkan dengan butiran ECH.</p></td></tr></tbody></table>
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Davis-Harrison, Rebecca L., Narjes Tavoosi, Vincent S. Pureza, and James H. Morrissey. "Phospholipid Synergy in Prothrombinase Activity." Blood 118, no. 21 (November 18, 2011): 1175. http://dx.doi.org/10.1182/blood.v118.21.1175.1175.
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Abstract Abstract 1175 Most steps in the blood coagulation cascade obligatorily take place on membrane surfaces and are dependent on the exposure of phosphatidylserine (PS). Previous studies from our lab and others have shown that phosphatidylethanolamine (PE) poorly supports clotting reactions by itself, but strongly synergizes with PS to promote several membrane-dependent steps in the blood clotting cascade, although the mechanism for PE-PS synergy has been unclear. We recently put forward a new mechanistic explanation – which we termed the ABC or Anything But Choline hypothesis – for how PS and PE synergize to enhance factor X (fX) activation by the factor VIIa-tissue factor complex (Tavoosi et al., J. Biol. Chem. 286:23247–53, 2011). The membrane contribution to this reaction is dominated by the affinity of fX for the membrane surface; since fX binds to membranes via its gamma-carboxyglutamate-rich (GLA) domain, the ABC hypothesis therefore focuses on the mechanisms by which GLA domains engage the phospholipid bilayer. We identified two main types of GLA domain-phospholipid interactions: a single phospho-L-serine-specific binding site in each GLA domain; and multiple ”phosphate-specific” interactions in which the phosphate groups of non-phosphatidylcholine phospholipids form coordination complexes with the tightly bound calcium ions in GLA domains. In the current study, we test the ABC hypothesis in the context of the prothrombinase complex – i.e., activation of prothrombin by the membrane-bound complex of fXa and factor Va (fVa). Using a variety of approaches including surface plasmon resonance analyses, we measured the contributions of varying phospholipid compositions to the membrane binding affinities of fXa, fVa and prothrombin, as well as to the enzymatic activity of prothrombinase. Our results suggest that phospholipid synergy in prothrombinase activity differs in certain respects from that observed for the factor VIIa-tissue factor complex. Not only did PS synergize with PE for enhancing the activity of prothrombinase, but phosphatidylglycerol (PG) and phosphatidylacid (PA) also synergized with PE, albeit more weakly than with PS (i.e., significantly higher levels of PG or PA in the presence of PE were required to achieve prothrombinase activities comparable to mixtures of PS and PE). In contrast, PE failed to synergize with either PG or PA to support fX activation by the factor VIIa-tissue factor complex. These differences primarily arise from differential membrane binding of the substrates for these two complexes (fX for factor VIIa-tissue factor and prothrombin for prothrombinase). The data suggest that the phospho-L-serine-specific binding site in the GLA domain of prothrombin may not be as stringent as that of fX, as high levels of PG or PA can substitute for PS in membrane binding of prothrombin but not for fX. This study provides further insights into the membrane's role in regulating blood clotting reactions, specifically the binding interactions between GLA domains and membrane surfaces. Disclosures: No relevant conflicts of interest to declare.
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Pisani, Antonio, Bianca Visciano, Roberta Russo, Giusi R. Mozzillo, Caterina Porto, Ilaria De Maggio, Roberta Russo, et al. "A novel GLA mutation in a Fabry family with glucose-6-phosphate dehydrogenase deficiency." Journal of Nephrology 25, no. 4 (2012): 582–85. http://dx.doi.org/10.5301/jn.5000073.
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Ciceri, Paola, Francesca Elli, Irene Brenna, Elisa Volpi, Diego Brancaccio, and Mario Cozzolino. "The Calcimimetic Calindol Prevents High Phosphate-Induced Vascular Calcification by Upregulating Matrix GLA Protein." Nephron Experimental Nephrology 122, no. 3-4 (2012): 75–82. http://dx.doi.org/10.1159/000349935.
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Bjørklund, Geir, Erik Svanberg, Maryam Dadar, David J. Card, Salvatore Chirumbolo, Dominic J. Harrington, and Jan Aaseth. "The Role of Matrix Gla Protein (MGP) in Vascular Calcification." Current Medicinal Chemistry 27, no. 10 (March 27, 2020): 1647–60. http://dx.doi.org/10.2174/0929867325666180716104159.
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Matrix Gla protein (MGP) is a vitamin K-dependent protein, which is synthesized in bone and many other mesenchymal cells, which is also highly expressed by vascular smooth muscle cells (VSMCs) and chondrocytes. Numerous studies have confirmed that MGP acts as a calcification-inhibitor although the mechanism of action is still not fully understood. The modulation of tissue calcification by MGP is potentially regulated in several ways including direct inhibition of calcium-phosphate precipitation, the formation of matrix vesicles (MVs), the formation of apoptotic bodies (ABs), and trans-differentiation of VSMCs. MGP occurs as four species, i.e. fully carboxylated (cMGP), under-carboxylated, i.e. poorly carboxylated (ucMGP), phosphorylated (pMGP), and non-phosphorylated (desphospho, dpMGP). ELISA methods are currently available that can detect the different species of MGP. The expression of the MGP gene can be regulated via various mechanisms that have the potential to become genomic biomarkers for the prediction of vascular calcification (VC) progression. VC is an established risk factor for cardiovascular disease and is particularly prevalent in those with chronic kidney disease (CKD). The specific action of MGP is not yet clearly understood but could be involved with the functional inhibition of BMP-2 and BMP-4, by blocking calcium crystal deposition and shielding the nidus from calcification.
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Lee, Ju-Young, Kwang-Hyeon Liu, Yunhi Cho, and Kun-Pyo Kim. "Enhanced Triacylglycerol Content and Gene Expression for Triacylglycerol Metabolism, Acyl-Ceramide Synthesis, and Corneocyte Lipid Formation in the Epidermis of Borage Oil Fed Guinea Pigs." Nutrients 11, no. 11 (November 18, 2019): 2818. http://dx.doi.org/10.3390/nu11112818.
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Triacylglycerol (TAG) metabolism is related to the acyl-ceramide (Cer) synthesis and corneocyte lipid envelope (CLE) formation involved in maintaining the epidermal barrier. Prompted by the recovery of a disrupted epidermal barrier with dietary borage oil (BO: 40.9% linoleic acid (LNA) and 24.0% γ-linolenic acid (GLA)) in essential fatty acid (EFA) deficiency, lipidomic and transcriptome analyses and subsequent quantitative RT-PCR were performed to determine the effects of borage oil (BO) on TAG content and species, and the gene expression related to overall lipid metabolism. Dietary BO for 2 weeks in EFA-deficient guinea pigs increased the total TAG content, including the TAG species esterified LNA, GLA, and their C20 metabolized fatty acids. Moreover, the expression levels of genes in the monoacylglycerol and glycerol-3-phosphate pathways, two major pathways of TAG synthesis, increased, along with those of TAG lipase, acyl-Cer synthesis, and CLE formation. Dietary BO enhanced TAG content, the gene expression of TAG metabolism, acyl-Cer synthesis, and CLE formation.
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Julien, M., D. Magne, M. Masson, M. Rolli-Derkinderen, O. Chassande, C. Cario-Toumaniantz, Y. Cherel, P. Weiss, and J. Guicheux. "Phosphate Stimulates Matrix Gla Protein Expression in Chondrocytes through the Extracellular Signal Regulated Kinase Signaling Pathway." Endocrinology 148, no. 2 (February 1, 2007): 530–37. http://dx.doi.org/10.1210/en.2006-0763.
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Whereas increasing evidence suggests that inorganic phosphate (Pi) may act as a signaling molecule in mineralization-competent cells, its mechanisms of action remain largely unknown. The aims of the present work were to determine whether Pi regulates expression of matrix Gla protein (MGP), a mineralization inhibitor, in growth plate chondrocytes and to identify the involved signaling pathways. Chondrogenic ATDC5 cells and primary growth plate chondrocytes were used. Messenger RNA and protein analyses were performed by quantitative PCR and Western blotting, respectively. The activation and role of MAPKs were, respectively, determined by Western blotting and the use of specific inhibitors. Immunohistological detection of ERK1/2 was performed in rib organ cultures from newborn mice. The results indicate that Pi markedly stimulates expression of MGP in ATDC5 cells and primary growth plate chondrocytes. Investigation of the involved intracellular signaling pathways reveals that Pi activates ERK1/2 in a cell-specific manner, because the stimulation was observed in ATDC5 and primary chondrocytes, MC3T3-E1 osteoblasts, and ST2 stromal cells, but not in L929 fibroblasts or C2C12 myogenic cells. Accordingly, immunohistological detection of ERK1/2 phosphorylation in rib growth plates revealed a marked signal in chondrocytes. Finally, a specific ERK1/2 inhibitor, UO126, blocks Pi-stimulated MGP expression in ATDC5 cells, indicating that ERK1/2 mediates, mainly, the effects of Pi. These data demonstrate, for the first time, that Pi regulates MGP expression in growth plate chondrocytes, thereby suggesting a key role for Pi and ERK1/2 in the regulation of bone formation.
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Julien, Marion, Solmaz Khoshniat, Aline Lacreusette, Martial Masson, Aline Bozec, Erwin Wagner, Pierre Weiss, David Magne, and Jerome Guicheux. "ERK1/2 and Fra-1 mediate phosphate-dependent stimulation of matrix Gla protein expression in osteoblasts." Bone 42 (March 2008): S23—S24. http://dx.doi.org/10.1016/j.bone.2007.12.026.
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Dai, Lu, Björn K. Meijers, Bert Bammens, Henriette de Loor, Leon J. Schurgers, Abdul Rashid Qureshi, Peter Stenvinkel, and Pieter Evenepoel. "Sevelamer Use in End-Stage Kidney Disease (ESKD) Patients Associates with Poor Vitamin K Status and High Levels of Gut-Derived Uremic Toxins: A Drug–Bug Interaction?" Toxins 12, no. 6 (May 27, 2020): 351. http://dx.doi.org/10.3390/toxins12060351.
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Gut microbial metabolism is not only an important source of uremic toxins but may also help to maintain the vitamin K stores of the host. We hypothesized that sevelamer therapy, a commonly used phosphate binder in patients with end-stage kidney disease (ESKD), associates with a disturbed gut microbial metabolism. Important representatives of gut-derived uremic toxins, including indoxyl sulfate (IndS), p-Cresyl sulfate (pCS), trimethylamine N-oxide (TMAO), phenylacetylglutamine (PAG) and non-phosphorylated, uncarboxylated matrix-Gla protein (dp-ucMGP; a marker of vitamin K status), were analyzed in blood samples from 423 patients (65% males, median age 54 years) with ESKD. Demographics and laboratory data were extracted from electronic files. Sevelamer users (n = 172, 41%) were characterized by higher phosphate, IndS, TMAO, PAG and dp-ucMGP levels compared to non-users. Sevelamer was significantly associated with increased IndS, PAG and dp-ucMGP levels, independent of age, sex, calcium-containing phosphate binder, cohort, phosphate, creatinine and dialysis vintage. High dp-ucMGP levels, reflecting vitamin K deficiency, were independently and positively associated with PAG and TMAO levels. Sevelamer therapy associates with an unfavorable gut microbial metabolism pattern. Although the observational design precludes causal inference, present findings implicate a disturbed microbial metabolism and vitamin K deficiency as potential trade-offs of sevelamer therapy.
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Julien, M., D. Magne, A. Clochard, M. Rolli-Derkinderen, O. Chassande, C. Cario-Toumaniantz, Y. Cherel, P. Weiss, and J. Guicheux. "72a Inorganic phosphate stimulates matrix GLA protein expression in growth plate chondrocytes through the ERK signaling pathway." Bone 38, no. 3 (March 2006): 35–36. http://dx.doi.org/10.1016/j.bone.2006.01.134.
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Stompór, Tomasz. "An Overview of the Pathophysiology of Vascular Calcification in Chronic Kidney Disease." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 27, no. 2_suppl (June 2007): 215–22. http://dx.doi.org/10.1177/089686080702702s37.
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Abnormalities of calcium–phosphate balance, with subsequent bone metabolism disorders, are among the key and earliest features of chronic kidney disease (CKD). Recently, another consequence of these abnormalities was brought to light—namely, vascular calcification. Most studies performed in patients on dialysis suggest that their vascular calcification is more advanced than that seen in the general population. Furthermore, the progression of vessel wall mineralization is much more dynamic in patients with CKD. Apart from the commonly assessed factors that promote vascular calcification, such as age, duration of dialysis, or poor control of calcium–phosphate status, several other factors have recently been identified. In the spectrum of substances involved in the regulation of the process of soft-tissue calcification, the most extensively studied in the nephrology literature are bone morphogenetic protein 7, osteoprotegerin, matrix Gla protein, fetuin-A, and the phosphatonins. Better understanding of the mechanisms underlying excess vascular mineralization have led to the development of promising new therapies.
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Jia, Guanghong, Ryan M. Stormont, Deepak M. Gangahar, and Devendra K. Agrawal. "Role of matrix Gla protein in angiotensin II-induced exacerbation of vascular calcification." American Journal of Physiology-Heart and Circulatory Physiology 303, no. 5 (September 1, 2012): H523—H532. http://dx.doi.org/10.1152/ajpheart.00826.2011.
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Vascular calcification predicts an increased risk for cardiovascular events in atherosclerosis, diabetes, and end-stage kidney diseases. Matrix Gla protein (MGP), an inhibitor of calcification, limits calcium phosphate deposition in the vessel wall. There are many factors contributing to the progression of atherosclerosis, including hypertension, hyperlipidemia, the renin-angiotensin system, and inflammation. Angiotensin II (ANG II) plays a crucial role in the atherogenic process through not only its pressor responses but also its growth-promoting and inflammatory effects. In this study, we investigated the role of MGP in ANG II-induced exacerbation of vascular calcification in human vascular smooth muscle cells (VSMCs). The expression of MGP, calcification, and apoptosis in human VSMCs were examined by Western blot analysis, real-time PCR, in situ terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling, and enzyme-linked immunosorbent assay, respectively. Increase in VSMC calcification in human atherosclerotic plaques upregulates MGP expression and apoptosis in a negative feedback manner. ANG II inhibited MGP expression in VSMCs via and in vitro in a dose- and time-dependent manner through ANG II type 1 receptor and NF-κB signaling pathway. Meanwhile, MGP inhibited the calcification, caspase-3 activity, activation of runt-related transcription factor 2, and release of inflammatory cytokines by VSMCs induced by calcification medium (2.5 mM Pi) and ANG II in vitro. These observations provide evidence that ANG II exacerbates vascular calcification through activation of the transcription factors, runt-related transcription factor 2 and NF-κB, and regulation of MGP, inflammatory cytokines expression in human VSMCs.
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Guitart Font, Emma, and Georg A. Sprenger. "Opening a Novel Biosynthetic Pathway to Dihydroxyacetone and Glycerol in Escherichia coli Mutants through Expression of a Gene Variant (fsaAA129S) for Fructose 6-Phosphate Aldolase." International Journal of Molecular Sciences 21, no. 24 (December 17, 2020): 9625. http://dx.doi.org/10.3390/ijms21249625.
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Phosphofructokinase (PFK) plays a pivotal role in glycolysis. By deletion of the genes pfkA, pfkB (encoding the two PFK isoenzymes), and zwf (glucose 6-phosphate dehydrogenase) in Escherichia coli K-12, a mutant strain (GL3) with a complete block in glucose catabolism was created. Introduction of plasmid-borne copies of the fsaA wild type gene (encoding E. coli fructose 6-phosphate aldolase, FSAA) did not allow a bypass by splitting fructose 6-phosphate (F6P) into dihydroxyacetone (DHA) and glyceraldehyde 3-phosphate (G3P). Although FSAA enzyme activity was detected, growth on glucose was not reestablished. A mutant allele encoding for FSAA with an amino acid exchange (Ala129Ser) which showed increased catalytic efficiency for F6P, allowed growth on glucose with a µ of about 0.12 h−1. A GL3 derivative with a chromosomally integrated copy of fsaAA129S (GL4) grew with 0.05 h−1 on glucose. A mutant strain from GL4 where dhaKLM genes were deleted (GL5) excreted DHA. By deletion of the gene glpK (glycerol kinase) and overexpression of gldA (of glycerol dehydrogenase), a strain (GL7) was created which showed glycerol formation (21.8 mM; yield approximately 70% of the theoretically maximal value) as main end product when grown on glucose. A new-to-nature pathway from glucose to glycerol was created.
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Silva, Ana P., Carla S. B. Viegas, Patrícia Guilherme, Nelson Tavares, Carolina Dias, Fátima Rato, Nélio Santos, et al. "Gla-Rich Protein, Magnesium and Phosphate Associate with Mitral and Aortic Valves Calcification in Diabetic Patients with Moderate CKD." Diagnostics 12, no. 2 (February 15, 2022): 496. http://dx.doi.org/10.3390/diagnostics12020496.
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Accelerated and premature cardiovascular calcification is a hallmark of chronic kidney disease (CKD) patients. Valvular calcification (VC) is a critical indicator of cardiovascular disease and all-cause mortality in this population, lacking validated biomarkers for early diagnosis. Gla-rich protein (GRP) is a cardiovascular calcification inhibitor recently associated with vascular calcification, pulse pressure, mineral metabolism markers and kidney function. Here, we examined the association between GRP serum levels and mitral and aortic valves calcification in a cohort of 80 diabetic patients with CKD stages 2–4. Mitral and aortic valves calcification were detected in 36.2% and 34.4% of the patients and associated with lower GRP levels, even after adjustments for age and gender. In this pilot study, univariate, multivariate and Poisson regression analysis, show that low levels of GRP and magnesium (Mg), and high levels of phosphate (P) are associated with mitral and aortic valves calcification. Receiver operating characteristic (ROC) curves showed that the area under the curve (AUC) values of GRP for mitral (0.762) and aortic (0.802) valves calcification were higher than those of Mg and P. These results suggest that low levels of GRP and Mg, and high levels of P, are independent and cumulative risk factors for VC in this population; the GRP diagnostic value might be potentially useful in cardiovascular risk assessment.
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Nagy, Annamária, Dávid Pethő, Rudolf Gesztelyi, Béla Juhász, György Balla, Zoltán Szilvássy, József Balla, and Tamás Gáll. "BGP-15 Inhibits Hyperglycemia-Aggravated VSMC Calcification Induced by High Phosphate." International Journal of Molecular Sciences 22, no. 17 (August 26, 2021): 9263. http://dx.doi.org/10.3390/ijms22179263.
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Vascular calcification associated with high plasma phosphate (Pi) level is a frequent complication of hyperglycemia, diabetes mellitus, and chronic kidney disease. BGP-15 is an emerging anti-diabetic drug candidate. This study was aimed to explore whether BGP-15 inhibits high Pi-induced calcification of human vascular smooth muscle cells (VSMCs) under normal glucose (NG) and high glucose (HG) conditions. Exposure of VSMCs to Pi resulted in accumulation of extracellular calcium, elevated cellular Pi uptake and intracellular pyruvate dehydrogenase kinase-4 (PDK-4) level, loss of smooth muscle cell markers (ACTA, TAGLN), and enhanced osteochondrogenic gene expression (KLF-5, Msx-2, Sp7, BMP-2). Increased Annexin A2 and decreased matrix Gla protein (MGP) content were found in extracellular vesicles (EVs). The HG condition markedly aggravated Pi-induced VSMC calcification. BGP-15 inhibited Pi uptake and PDK-4 expression that was accompanied by the decreased nuclear translocation of KLF-5, Msx-2, Sp7, retained VSMC markers (ACTA, TAGLN), and decreased BMP-2 in both NG and HG conditions. EVs exhibited increased MGP content and decreased Annexin A2. Importantly, BGP-15 prevented the deposition of calcium in the extracellular matrix. In conclusion, BGP-15 inhibits Pi-induced osteochondrogenic phenotypic switch and mineralization of VSMCs in vitro that make BGP-15 an ideal candidate to attenuate both diabetic and non-diabetic vascular calcification.
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Silva, Ana P., Carla S. B. Viegas, Filipa Mendes, Ana Macedo, Patrícia Guilherme, Nelson Tavares, Carolina Dias, et al. "Gla-Rich Protein (GRP) as an Early and Novel Marker of Vascular Calcification and Kidney Dysfunction in Diabetic Patients with CKD: A Pilot Cross-Sectional Study." Journal of Clinical Medicine 9, no. 3 (February 27, 2020): 635. http://dx.doi.org/10.3390/jcm9030635.
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Vascular calcification (VC) is one of the strongest predictors of cardiovascular risk in chronic kidney disease (CKD) patients. New diagnostic/prognostic tools are required for early detection of VC allowing interventional strategies. Gla-rich protein (GRP) is a cardiovascular calcification inhibitor, whose clinical utility is here highlighted. The present study explores, for the first time, correlations between levels of GRP in serum with CKD developmental stage, mineral metabolism markers, VC and pulse pressure (PP), in a cohort of 80 diabetic patients with mild to moderate CKD (stages 2–4). Spearman’s correlation analysis revealed a positive association of GRP serum levels with estimated glomerular filtration rate (eGFR) and α-Klotho, while a negative correlation with phosphate (P), fibroblast growth factor 23 (FGF-23), vascular calcification score (VCS), PP, calcium (x) phosphate (CaxP) and interleukin 6 (IL-6). Serum GRP levels were found to progressively decrease from stage 2 to stage 4 CKD. Multivariate analysis identified low levels of eGFR and GRP, and high levels of FGF-23 associated with both the VCS and PP. These results indicate an association between GRP, renal dysfunction and CKD-mineral and bone disorder. The relationship between low levels of GRP and vascular calcifications suggests a future, potential utility for GRP as an early marker of vascular damage in CKD.
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Zhao, Jingsong, Nobuhito Araki, and Satoru K. Nishimoto. "Quantitation of matrix Gla protein mRNA by competitive polymerase chain reaction using glyceraldehyde-3-phosphate dehydrogenase as an internal control." Gene 155, no. 2 (April 1995): 159–65. http://dx.doi.org/10.1016/0378-1119(94)00895-y.
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Neradova, Aegida, Grzegorz Wasilewski, Selene Prisco, Peter Leenders, Marjolein Caron, Tim Welting, Bert van Rietbergen, et al. "Combining phosphate binder therapy with vitamin K2 inhibits vascular calcification in an experimental animal model of kidney failure." Nephrology Dialysis Transplantation 37, no. 4 (October 30, 2021): 652–62. http://dx.doi.org/10.1093/ndt/gfab314.
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ABSTRACT Background Hyperphosphataemia is strongly associated with cardiovascular disease and mortality. Recently, phosphate binders (PBs), which are used to bind intestinal phosphate, have been shown to bind vitamin K, thereby potentially aggravating vitamin K deficiency. This vitamin K binding by PBs may offset the beneficial effects of phosphate reduction in reducing vascular calcification (VC). Here we assessed whether combining PBs with vitamin K2 supplementation inhibits VC. Methods We performed 3/4 nephrectomy in rats, after which warfarin was given for 3 weeks to induce vitamin K deficiency. Next, animals were fed a high phosphate diet in the presence of low or high vitamin K2 and were randomized to either control or one of four different PBs for 8 weeks. The primary outcome was the amount of thoracic and abdominal aorta VC measured by high-resolution micro-computed tomography (µCT). Vitamin K status was measured by plasma MK7 levels and immunohistochemically analysed in vasculature using uncarboxylated matrix Gla protein (ucMGP) specific antibodies. Results The combination of a high vitamin K2 diet and PB treatment significantly reduced VC as measured by µCT for both the thoracic (P = 0.026) and abdominal aorta (P = 0.023), compared with MK7 or PB treatment alone. UcMGP stain was significantly more present in the low vitamin K2–treated groups in both the thoracic (P < 0.01) and abdominal aorta (P < 0.01) as compared with high vitamin K2–treated groups. Moreover, a high vitamin K diet and PBs led to reduced vascular oxidative stress. Conclusion In an animal model of kidney failure with vitamin K deficiency, neither PB therapy nor vitamin K2 supplementation alone prevented VC. However, the combination of high vitamin K2 with PB treatment significantly attenuated VC.
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Cooper, DW, PG Johnston, JL Vandeberg, and ES Robinson. "X-Chromosome Inactivation in Marsupials." Australian Journal of Zoology 37, no. 3 (1989): 411. http://dx.doi.org/10.1071/zo9890411.
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Marsupial (metatherian) mammals resemble their eutherian ('placental') counterparts in having inacti- vation of one of the two X chromosomes in the soma and premeiotic germ cells of their females. The marsupial X-inactivation system differs from the eutherian system in two respects: firstly, inactivation occurs for the paternally derived allele, i.e. it is not random, and secondly it is often incomplete. Data are available for four X-linked loci, all controlling enzyme structure: glucose-6- phosphate dehydrogenase (G6PD), phosphoglycerate kinase 1 (PGKl), alpha-galactosidase (GLA) and hypoxanthine phosphoribosyl transferase (HPRT). Both the G6PD and PGKl loci exhibit incomplete X-chromosome inactivation. The pattern of partial expression differs from tissue to tissue and from species to species. One of the two X chromosomes exhibits late replication, even in cells where a paternally derived gene is partly active, showing that late replication and absence of transcription are not completely correlated. Sex chromatin bodies are not as easily found as in some eutherians. In marsupials they are most clearly demonstrable in species with small Y chromosomes. Investigations into X-inactivation in early development have just begun. Absence of inactivation at the G6PD locus in yolk sac of a kangaroo has been observed. All other tissues exhibited complete paternal X-inacti- vation for G6PD. In a dasyurid, GLA showed complete paternal X-inactivation in all embryonic and extra-embryonic tissues. The role, if any, of methylation of cytosine residues in CpG pairs in the maintenance of X-inactivation in marsupials is unclear. Preliminary evidence indicates that sex-specific differences in methylation of sex linked genes do exist in marsupials.
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Petrauskiene, Vaida, Ruta Vaiciuniene, Vytautas Kuzminskis, Edita Ziginskiene, Saulius Grazulis, Egle Jonaitiene, Erika Skrodeniene, and Inga Arune Bumblyte. "Associations of vascular calcification, calcium phosphate disturbances, FGF 23 and Matrix Gla protein with mortality of hemodialysis patients: one center cohort study." Revista Romana de Medicina de Laborator 26, no. 4 (October 1, 2018): 451–60. http://dx.doi.org/10.2478/rrlm-2018-0034.
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Abstract Background and objectives: Vascular calcification (VC) is one of the factors associated with mortality in hemodialysis (HD) patients. The purpose of the study was to assess associations between prevalent VC and disturbances of calcium-phosphate metabolism as well as changes in vitamin D (25(OH)D), FGF 23 and MGP levels and to evaluate the possible impact of VC and changes of these biomarkers on survival in HD patients. Methods: The study population consisted of 81 prevalent patients in the hemodialysis unit of Hospital of Lithuanian University of Health Sciences Kaunas Clinics. A simple vascular calcification score (SVCS) was evaluated as it is described by Adragao et al. 25(OH)D (nmol/L), FGF 23 (ng/L) and MGP (ng/mL) were measured and analysed. Results: Patients were divided into two groups: SVCS<3 (31 patient (38.3%) and SVCS ≥3 (50 patients (61.7%)). In multivariate logistic regression, age (odds ratio 1.062, 95% CI [1.024-1.1] p=0.001) and diabetes (odds ratio 6.9, 95% CI [1.5-31], p=0.012) were associated with SVCS ≥3. The multivariate logistic regression revealed the highest negative impact of SVCS ≥3, age and 25(OH)D level for death risk. Conclusion: VC in HD patients is highly influenced by age and presence of diabetes and associated with higher risk of death. No significant association was found between MGP and FGF 23 and VC as well as between these two biomarkers and risk of death. Lower 25(OH)D levels were associated with mortality in this dialysis patients cohort.
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Hermans, Marc M. H., Cees Vermeer, Jeroen P. Kooman, Vincent Brandenburg, Markus Ketteler, Ulrich Gladziwa, Pieter L. Rensma, Karel M. L. Leunissen, and Leon J. Schurgers. "Undercarboxylated Matrix GLA Protein Levels Are Decreased in Dialysis Patients and Related to Parameters of Calcium-Phosphate Metabolism and Aortic Augmentation Index." Blood Purification 25, no. 5-6 (2007): 395–401. http://dx.doi.org/10.1159/000108629.
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Price, Paul A., Jeffrey M. Caputo, and Matthew K. Williamson. "Bone Origin of the Serum Complex of Calcium, Phosphate, Fetuin, and Matrix Gla Protein: Biochemical Evidence for the Cancellous Bone-Remodeling Compartment." Journal of Bone and Mineral Research 17, no. 7 (July 1, 2002): 1171–79. http://dx.doi.org/10.1359/jbmr.2002.17.7.1171.
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Roy, M. E., and S. K. Nishimoto. "Matrix Gla protein binding to hydroxyapatite is dependent on the ionic environment: calcium enhances binding affinity but phosphate and magnesium decrease affinity." Bone 31, no. 2 (August 2002): 296–302. http://dx.doi.org/10.1016/s8756-3282(02)00821-9.
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Yaker, Linda, Saïd Kamel, Jérôme Ausseil, and Agnès Boullier. "Effects of Chronic Kidney Disease and Uremic Toxins on Extracellular Vesicle Biology." Toxins 12, no. 12 (December 21, 2020): 811. http://dx.doi.org/10.3390/toxins12120811.
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Vascular calcification (VC) is a cardiovascular complication associated with a high mortality rate, especially in patients with diabetes, atherosclerosis or chronic kidney disease (CKD). In CKD patients, VC is associated with the accumulation of uremic toxins, such as indoxyl sulphate or inorganic phosphate, which can have a major impact in vascular remodeling. During VC, vascular smooth muscle cells (VSMCs) undergo an osteogenic switch and secrete extracellular vesicles (EVs) that are heterogeneous in terms of their origin and composition. Under physiological conditions, EVs are involved in cell-cell communication and the maintenance of cellular homeostasis. They contain high levels of calcification inhibitors, such as fetuin-A and matrix Gla protein. Under pathological conditions (and particularly in the presence of uremic toxins), the secreted EVs acquire a pro-calcifying profile and thereby act as nucleating foci for the crystallization of hydroxyapatite and the propagation of calcification. Here, we review the most recent findings on the EVs’ pathophysiological role in VC, the impact of uremic toxins on EV biogenesis and functions, the use of EVs as diagnostic biomarkers and the EVs’ therapeutic potential in CKD.
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Rzewuska-Lech, Ewa, Muthuvel Jayachandran, Lorraine A. Fitzpatrick, and Virginia M. Miller. "Differential effects of 17β-estradiol and raloxifene on VSMC phenotype and expression of osteoblast-associated proteins." American Journal of Physiology-Endocrinology and Metabolism 289, no. 1 (July 2005): E105—E112. http://dx.doi.org/10.1152/ajpendo.00366.2004.
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Several studies demonstrate an association between osteoporosis and arterial calcific disease, both of which being common in elderly women. Estradiol and raloxifene, a selective estrogen receptor modulator, prevent bone loss in postmenopausal women. Little is known regarding how these agents affect arterial calcification. The aim of this study was to determine whether or not 17β-estradiol and raloxifene reduced vascular smooth muscle cell (VSMC) differentiation and expression of bone-associated proteins during phosphate-induced calcification in vitro. Aortic VSMC were cultured from adult, gonadally intact, and ovariectomized (OVX) female pigs. Calcifying medium was added, and cells were treated with solvent (control), 17β-estradiol (E2), or raloxifene. Extent of calcification and phenotypic expression of bone-associated proteins [matrix gla protein (MGP), osteoprotegerin (OPG), and bone sialoprotein (BSP)] were examined at 3-day intervals over 2 wk. Calcium content increased in all groups but was greater in VSMC derived from intact compared with OVX animals. E2 reduced calcification and preserved a contractile phenotype. Expression of OPG significantly decreased with time; this decrease was significantly greater in VSMC derived from OVX compared with gonadally intact pigs. E2 and raloxifene preserved expression of OPG only in VSMC from intact pigs. Expression of MGP increased significantly with time and was not affected by E2 or raloxifene treatments. E2 treatment significantly inhibited synthesis of BSP in cells from both groups. In conclusion, E2 slows differentiation of VSMC induced by excess phosphate. Effectiveness of raloxifene to preserve expression of bone cell-associated proteins depends on the hormonal status of the tissue donor.
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Zhou, Ye-Bo, Shao-Ju Jin, Yan Cai, Xu Teng, Li Chen, Chao-Shu Tang, and Yong-Fen Qi. "Lanthanum Acetate Inhibits Vascular Calcification Induced by Vitamin D3 Plus Nicotine in Rats." Experimental Biology and Medicine 234, no. 8 (August 2009): 908–17. http://dx.doi.org/10.3181/0811-rm-346.
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Lanthanum, a rare earth element, has been used to decrease serum phosphorus level in patients with chronic renal disease and hyperphosphatemia. We aimed to observe the effect and mechanism of two doses of lanthanum acetate (375 and 750 mg/kg/day) on vascular calcification induced by vitamin D3 plus nicotine treatment in rats for 4 weeks. As compared with control rats, rats with calcification showed widespread calcified nodules and irregular elastic fibers in calcified aorta on von Kossa calcium staining and increased aortic calcium and phosphorus contents, alkaline phosphatase (ALP) activity and bone-related protein expressions for osteopontin (OPN) and type III sodium dependent phosphate cotransporter Pit-1 (Pit-1). After treatment with either dose of lanthanum acetate, the calcified nodules and degree of irregular elastic fibers decreased in aortas. Lanthanum acetate at 750 mg/kg/day was more effective than 375 mg/kg/day in lessening vascular calcification by significantly reducing plasma phosphorus level, calcium × phosphorus product and ALP activity, by 30.3%, 28.6%, and 68.6%, respectively; reducing aortic phosphorus and calcium contents and ALP activity, by 48%, 53.1%, and 63.5% (all P < 0.01), respectively; reducing aortic mRNA level of OPN and Pit-1, by 55.8% ( P < 0.01) and 38.8% ( P < 0.05) and protein level of OPN and Pit-1, by 37.2% and 27.2% (both P < 0.01), respectively; and increasing carboxylated matrix Gla-protein (MGP) protein expression by 33.7% ( P < 0.05), as compared with rats treated with vitamin D3 and nicotine alone. Lanthanum acetate could effectively inhibit the pathogenesis of vascular calcification.
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Frustaci, Andrea, Romina Verardo, Rossella Scialla, Giulia Bagnato, Margherita Verardo, Maria Alfarano, and Matteo A. Russo. "Downregulation of Mannose-6-Phosphate Receptors in Fabry Disease Cardiomyopathy: A Potential Target for Enzyme Therapy Enhancement." Journal of Clinical Medicine 11, no. 18 (September 16, 2022): 5440. http://dx.doi.org/10.3390/jcm11185440.
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Background: The efficacy of enzyme replacement therapy (ERT) in mobilizing globotryaosylceramide (GB-3) from Fabry cardiomyocytes is limited. The mechanism involved is still obscure. Methods: Assessment of M6Pr, M6Pr-mRNA, and Ubiquitin has been obtained by Western blot analysis and real-time PCR of frozen endomyocardial biopsy samples, from 17 pts with FD, various degree of left ventricular hypertrophy, and maximal wall thickening (MWT) from 11.5 and 20 mm. The diagnosis and severity of FDCM followed definitions of GLA mutation, α-galactosidase A enzyme activity, cardiac magnetic resonance, and left ventricular endomyocardial biopsy with the quantification of myocyte hypertrophy and the extent of Gb-3 accumulation. All patients have received alpha or beta agalsidase for ≥3 years without a reduction in LV mass nor an increase in T1 mapping at CMR. Controls were surgical biopsies from 15 patients undergoing mitral valve replacement. Results: Protein analysis showed mean M6Pr in FDCM to be 5.4-fold lower than in a normal heart (4289 ± 6595 vs. 23,581 ± 4074, p = 0.0996) (p < 0.001): specifically, 9-fold lower in males, p = 0.009, (p < 0.001) and 3-fold lower in females, p = 0.5799, (p < 0.001) showing, at histology, a mosaic of normal and diseased cells. M6Pr-mRNA expression was normal, while ubiquitin showed an increase of 4.6 fold vs. controls (13,284 ± 1723 vs. 2870 ± 690, p = 0.001) suggesting that ubiquitin-dependent post-translational degradation is likely responsible for the reduction of M6Pr in FDCM. Conclusion: M6Pr expression is remarkably reduced in FDCM as a likely result of post-translational degradation. This may explain the reduced efficacy of ERT and be a therapeutic target for the enhancement of ERT activity.
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Cui, Heng-Lin, Xin Yang, Xia Gao, and Xue-Wei Xu. "Halobellus clavatus gen. nov., sp. nov. and Halorientalis regularis gen. nov., sp. nov., two new members of the family Halobacteriaceae." International Journal of Systematic and Evolutionary Microbiology 61, no. 11 (November 1, 2011): 2682–89. http://dx.doi.org/10.1099/ijs.0.025841-0.
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Four halophilic archaeal strains, designated TNN18T, TBN12, TNN28T and TBN19, were isolated from brines sampled from two artificial marine solar salterns in eastern China. Strains TNN18T and TNN28T were isolated from the Tainan marine solar saltern, whereas strains TBN12 and TBN19 were from the Taibei marine solar saltern. Colonies of the four strains were red-pigmented and their cells were pleomorphic, motile, Gram-reaction-negative rods. Strains TNN18T and TBN12 were able to grow at 25–50 °C (optimum 37 °C), in 10–30 % (w/v) NaCl (optimum 15 %), with 0–1.0 M MgCl2 (optimum 0.05 M) and at pH 5.5–9.0 (optimum pH 7.0–7.5), while strains TNN28T and TBN19 were able to grow at 20–50 °C (optimum 37 °C), in 15-30 % (w/v) NaCl (optimum 18–20 %), in 0.005–1.0 M MgCl2 (optimum 0.01–0.3 M) and at pH 6.0–9.0 (optimum pH 7.0–7.5). Cells of these strains lyse in distilled water; minimal NaCl concentrations to prevent cell-lysis are 10 % (w/v) for strains TNN18T and TBN12 and 12 % (w/v) for strains TNN28T and TBN19. The major polar lipids of strains TNN18T and TBN12 were phosphatidylglycerol (PG), phosphatidylglycerol phosphate methyl ester (PGP-Me), phosphatidylglycerol sulfate (PGS) and one major glycolipid (GL1), which was chromatographically identical to sulfated mannosyl glucosyl diether (S-DGD-1). Minor amounts of other lipids (GL0, GL2, GL3 and GL4) were also detectable. The polar lipid profiles of strains TNN28T and TBN19 contained PG, PGP-Me, GL1, which was chromatographically identical to S-DGD-1, and three to four minor unidentified glycolipids (GL2–GL5). Phylogenetic analyses revealed that strains TNN18T and TBN12 formed a distinct clade with strains of the closest related species, Haloquadratum walsbyi (91.5–91.8 % 16S rRNA gene sequence similarity) and strains TNN28T and TBN19 formed a distinct clade with strains of the species Halosimplex carlsbadense (89.9–93.3 % similarity) and two members of the genus Halorhabdus (92.5–93.3 % similarity). The DNA G+C contents of strains TNN18T, TBN12, TNN28T and TBN19 were 61.5, 62.4, 61.9 and 61.5 mol%, respectively. DNA–DNA hybridization values between strains TNN18T and TBN12, and strains TNN28T and TBN19 were 82.9 % and 88.2 %, respectively. The phenotypic, chemotaxonomic and phylogenetic properties suggest that the four strains represent two novel species of two new genera within the family Halobacteriaceae, for which the names Halobellus clavatus gen. nov., sp. nov. (type strain TNN18T = CGMCC 1.10118T = JCM 16424T) and Halorientalis regularis gen. nov., sp. nov. (type strain TNN28T = CGMCC 1.10123T = JCM 16425T) are proposed.
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Lu, S. E., R. A. Henn, and D. H. Nagel. "First Report of Ear Soft Rot of Corn (Zea mays) Caused by Burkholderia gladioli in the United States." Plant Disease 91, no. 11 (November 2007): 1514. http://dx.doi.org/10.1094/pdis-91-11-1514c.
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During the summer of 2005, an uncharacterized disease was observed on sweet corn ‘Mirai 301BC’ commercially grown in Sunflower County, Mississippi. Initial symptoms developing at the base of the ear on interior husk leaves were brown, water-soaked, irregular lesions. These gradually enlarged up to 10 cm in diameter. Market value was significantly affected when the corn ears had visible symptoms of this disease. Bacterial cell streaming was observed at a magnification of ×675 from the diseased husk. A bacterium was consistently isolated from lesions on nutrient broth yeast (NBY) agar. Colonies on NBY were yellowish white, slightly convex, shiny, and circular with entire margins. Isolates MS102 and MS103, which were chosen for further characterization, were gram negative, lacked arginine dihydrolase, did not produce fluorescent pigment on Pseudomonas F medium, accumulated poly-β-hydroxybutyrate, and grew aerobically. The isolates were able to utilize l-arabinose, d-mannitol, N-acetylglucosamine, capric acid, malic acid, adipic acid, and phenylacetic acid, but not d-maltose. These characteristics are the same as those described previously for Burkholderia gladioli (3). Analysis of fatty acid methyl ester profiles (Sherlock version TSBA 4.10; Microbial Identification System, Newark, DE) characterized the isolates as B. gladioli (similarity indices: 0.23 to 0.38) and revealed that they have C16:0 3OH, the most characteristic fatty acid for the genus Burkholderia. Confirmation was made by PCR amplification of the nearly complete16S rRNA gene (1,471 bp; GenBank Accession No. EU053154) using universal primers (forward: 5′-AGAGTTTGATCCTGGCTCAG and reverse: 5′-GGCTACCTTGTTACGACTTC). DNA sequence analysis demonstrated that the 16S rRNA gene of the bacterium shared highest identities (99.4 to 99.6%) with that of B. gladioli strains 321gr-6, 223gr-1, and S10 (4). A PCR product (approximately 300 bp) characteristic of B. gladioli also was obtained from both isolates using species-specific primers GLA-f and GLA-r (2). To confirm pathogenicity, cell suspensions (108 CFU/ml in phosphate buffer) of isolates MS102 and MS103 were injected into interior husk leaves of field-grown sweet corn with a 20-gauge needle and syringe (2 ml per ear). Control corn ear husks were injected with phosphate buffer. After 3 days, ear rot symptoms were observed on all plants inoculated with the isolates but not those injected with phosphate buffer. Cell suspension of isolates dropped on nonwounded husks also incited the same symptoms as those inoculated with the syringe. Koch's postulates were fulfilled with reisolation from the inoculated tissues. The identity of the reisolated pathogen was proved by sequencing the 16S rRNA gene. This disease was previously reported in Brazil (1). To our knowledge, this is the first report of B. gladioli causing a disease of corn in the United States. Although the impact of this disease was not observed from 2005 to 2006 because of dry weather and rotation to other crops in the affected field, there is a potential that the bacterium could become established in corn-producing areas as a member of the corn ear rot complex if environmental conditions are favorable. Reference: (1) I. M. G. Almeida et al. Arq. Inst. Biol. Sao Paulo 66:141, 1999. (2) N. Furuya et al. J. Gen. Plant Pathol. 68:220, 2002. (3) M. Gillis et al. Int. J. Syst. Bacteriol. 45:274, 1995. (4) R. Nandakumar et al. Phytopathology (Abstr.) 95(suppl.):S73, 2005.
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Beyer, Stefan, Gerd Mayer, and Wolfgang Piepersberg. "The StrQ protein encoded in the gene cluster for 5'-hydroxystreptomycin of Streptomyces glaucescens GLA.0 is a alpha- D-glucose-1-phosphate cytidylyltransferase (CDP- D-glucose synthase)." European Journal of Biochemistry 258, no. 3 (December 15, 1998): 1059–67. http://dx.doi.org/10.1046/j.1432-1327.1998.2581059.x.
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Sowers, Kurt M., and Melvin R. Hayden. "Calcific Uremic Arteriolopathy: Pathophysiology, Reactive Oxygen Species and Therapeutic Approaches." Oxidative Medicine and Cellular Longevity 3, no. 2 (2010): 109–21. http://dx.doi.org/10.4161/oxim.3.2.11354.
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Calcific uremic arteriolopathy (CUA)/calciphylaxis is an important cause of morbidity and mortality in patients with chronic kidney disease requiring renal replacement. Once thought to be rare, it is being increasingly recognized and reported on a global scale. The uremic milieu predisposes to multiple metabolic toxicities including increased levels of reactive oxygen species and inflammation. Increased oxidative stress and inflammation promote this arteriolopathy by adversely affecting endothelial function resulting in a prothrombotic milieu and significant remodeling effects on vascular smooth muscle cells. These arteriolar pathological effects include intimal hyperplasia, inflammation, endovascular fibrosis and vascular smooth muscle cell apoptosis and differentiation into bone forming osteoblast-like cells resulting in medial calcification. Systemic factors promoting this vascular condition include elevated calcium, parathyroid hormone and hyperphosphatemia with consequent increases in the calcium × phosphate product. The uremic milieu contributes to a marked increased in upstream reactive oxygen species—oxidative stress and subsequent downstream increased inflammation, in part, via activation of the nuclear transcription factor NFκB and associated downstream cytokine pathways. Consitutive anti-calcification proteins such as Fetuin-A and matrix GLA proteins and their signaling pathways may be decreased, which further contributes to medial vascular calcification. The resulting clinical entity is painful, debilitating and contributes to the excess morbidity and mortality associated with chronic kidney disease and end stage renal disease. These same histopathologic conditions also occur in patients without uremia and therefore, the term calcific obliterative arteriolopathy could be utilized in these conditions.
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Francini, G., S. Gonnelli, R. Petrioli, F. Conti, P. Paffetti, and C. Gennari. "Treatment of bone metastases with dichloromethylene bisphosphonate." Journal of Clinical Oncology 10, no. 4 (April 1992): 591–98. http://dx.doi.org/10.1200/jco.1992.10.4.591.
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PURPOSE The study was undertaken to evaluate the effects of dichloromethylene bisphosphonate (Cl2MDP) on osteolytic and osteoblastic bone lesions from a variety of tumoral primary sites and to investigate the in vivo mechanism underlying the action of this drug. PATIENTS AND METHODS Seventy-six patients participated in the current study: 59 had predominantly osteolytic lesions and 17 osteoblastic metastases. Sixteen patients had hypercalcemia. All of the patients received 300 mg of Cl2MDP intravenously (IV) for 7 days and then 200 mg of Cl2MDP intramuscularly (IM) for 14 days. Biochemical parameters were measured in the patients before the start of treatment and 3, 7, 14, and 21 days after beginning treatment. After the withdrawal of parenteral Cl2MDP, 59 patients with predominantly osteolytic lesions were then randomized to receive chemotherapy alone (group A, 29 cases) or chemotherapy plus Cl2MDP given at an oral dose of 1,200 mg/d (group B, 30 cases). RESULTS Serum calcium (Ca), urinary calcium (UCa) phosphate (UPO4), and hydroxyproline (HOP) excretion levels significantly decreased in all patients, whereas no significant changes occurred in serum alkaline phosphatase (AlkPh) and bone Gla-protein (BGP) levels. In 56 patients with painful bone lesions, a progressive analgesic effect was observed mainly between day 7 and day 14. In patients with predominantly osteoblastic metastases, the Cl2MDP treatment led to a more evident hypocalcemia and an increase in both AlkPh and BGP. However, in the majority of these patients the hypocalcemia was corrected by the concurrent use of effective cytotoxic treatments capable of reducing osteoblast stimulation. During 6 months of follow-up, two pathologic fractures occurred in patients of group A, and none occurred in patients of group B. CONCLUSIONS We conclude that Cl2MDP was effective in patients presenting bone metastases with and without hypercalcemia. Care should be taken particularly in those patients with mixed metastases when the sclerotic component is predominant, as the drug may enhance the possibility of hypocalcemia, which is generally corrected by effective cytotoxic drugs. Therefore, Cl2MDP can be considered a valuable support in the treatment of bone metastases.
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Sekhri, Arunabh, Robert G. Lerner, Wilbert S. Aronow, Chandrasekar Palaniswamy, Chul Ahn, Tarunjit Singh, Rasham Sandhu, and John A. McClung. "Warfarin Use May Be Associated with Increase Prevalence of Valvular Calcification." Blood 114, no. 22 (November 20, 2009): 3137. http://dx.doi.org/10.1182/blood.v114.22.3137.3137.
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Abstract Abstract 3137 Poster Board III-74 Background Warfarin affects the synthesis and function of the matrix Gla protein, a vitamin K–dependent protein, which is a potent inhibitor of tissue calcification. We aimed to study the association of use of warfarin with calcification of the mitral valve, mitral annulus, and aortic valve. Methods We reviewed 1155 patient's charts with a diagnosis of nonvalvular atrial fibrillation. Based on the chart review, patients were grouped into the warfarin group and the no warfarin group. The following parameters were recorded in both groups: age, ethnicity, glomerular filtration rate, calcium-phosphate product, lipid profile, coronary artery disease, diabetes, hypertension and intake of medications including aspirin, angiotensin converting enzyme inhibitors, angiotensin receptor blockers, statins, and beta blockers. All the echocardiograms were analyzed by two cardiologists blinded to the clinical details of subjects but alerted to evaluate for the presence of mitral valve calcium (MVC), mitral annular calcium (MAC), aortic valve calcium (AVC), or any of the three. Stepwise logistic regression analysis was used to identify significant independent risk factors associated with any calcification using twenty five variables. Results Out of 1155 patient records reviewed, 725(63%) were in the warfarin group and 430(37%) were in the no warfarin group. MVC, MAC, or AVC was present in 473 of 725 patients (65%) on warfarin versus 225 of 430 patients (52%) not on warfarin (p<0.0001). Stepwise logistic regression analysis showed significant independent risk factors for any valve calcification were use of warfarin (Odds ratio 1.972, p-value< 0.001), age (Odds ratio 1.078 per one year increase, p-value <0.001), dyslipidemia (Odds ratio 0.235,p-value <0.001), calcium-phosphate product (Odds ratio 1.015, p-value 0.024), and coronary artery disease ( Odds ratio 13.563, p-value <0.0001). Conclusion Warfarin intake is associated with a significantly higher prevalence of MVC, MAC or AVC. Further studies are needed to confirm this association and the duration of warfarin intake for development of calcification. A pilot study has been started to study the effect of oral vitamin K on valvular calcification. Disclosures Off Label Use: Oral Vitamin K in preventing calcification.
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Jansz, Thijs T., Franka E. van Reekum, Akin Özyilmaz, Pim A. de Jong, Franciscus T. J. Boereboom, Tiny Hoekstra, Marianne C. Verhaar, and Brigit C. van Jaarsveld. "Coronary Artery Calcification in Hemodialysis and Peritoneal Dialysis." American Journal of Nephrology 48, no. 5 (2018): 369–77. http://dx.doi.org/10.1159/000494665.
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Background: Vascular calcification is seen in most patients on dialysis and is strongly associated with cardiovascular mortality. Vascular calcification is promoted by phosphate, which generally reaches higher levels in hemodialysis than in peritoneal dialysis. However, whether vascular calcification develops less in peritoneal dialysis than in hemodialysis is currently unknown. Therefore, we compared coronary artery calcification (CAC), its progression, and calcification biomarkers between patients on hemodialysis and peritoneal dialysis. Methods: We measured CAC in 134 patients who had been treated exclusively with hemodialysis (n = 94) or peritoneal dialysis (n = 40) and were transplantation candidates. In 57 of them (34 on hemodialysis and 23 on peritoneal dialysis), we also measured CAC progression annually up to 3 years and the inactive species of desphospho-uncarboxylated matrix Gla protein (dp-ucMGP), fetuin-A, osteoprotegerin. We compared CAC cross-sectionally with Tobit regression. CAC progression was compared in 2 ways: with linear mixed models as the difference in square root transformed volume score per year (ΔCAC SQRV) and with Tobit mixed models. We adjusted for potential confounders. Results: In the cross-sectional cohort, CAC volume scores were 92 mm3 in hemodialysis and 492 mm3 in peritoneal dialysis (adjusted difference 436 mm3; 95% CI –47 to 919; p = 0.08). In the longitudinal cohort, peritoneal dialysis was associated with significantly more CAC progression defined as ΔCAC SQRV (adjusted difference 1.20; 95% CI 0.09 to 2.31; p = 0.03), but not with Tobit mixed models (adjusted difference in CAC score increase per year 106 mm3; 95% CI –140 to 352; p = 0.40). Peritoneal dialysis was associated with higher osteoprotegerin (adjusted p = 0.02) but not with dp-ucMGP or fetuin-A. Conclusions: Peritoneal dialysis is not associated with less CAC or CAC progression than hemodialysis, and perhaps with even more progression. This indicates that vascular calcification does not develop less in peritoneal dialysis than in hemodialysis.
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Kobayashi, Yoshiyuki, Nobory Ishida, Masami Arai, Masao Shiozaki, Tetsuo Hiraoka, Masahiro Nishijima, Sayuri Kuge, Toshiaki Otsuka, and Yuzuru Akamatsu. "Syntheses of 2,6-dideoxy-6-fluoro-2-[(3R and 3S)-3- hydroxytetradecanamido]-3-O-[(3R)-3-(tetradecanoyloxy)- tetradecanoyl]-d-glucopyranose 4-(dihydrogen phosphate) and 2-deoxy-2-[(3R and 3S)-3-hydroxytetradecanamido]- 3-O-[(3R)-3-(tetradecanoyloxy)tetradecanoyl]-α-d-glucopyranosyl fluoride 4-(dihydrogen phosphate): fluorosugar analogues of GLA-60." Carbohydrate Research 222 (December 1991): 83–97. http://dx.doi.org/10.1016/0008-6215(91)89008-4.
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Banko, T. J., and C. X. Hong. "Evaluation of Nutrient Phosphite for the Control of Phytophthora Shoot Blight on Annual Vinca." Journal of Environmental Horticulture 22, no. 1 (March 1, 2004): 41–44. http://dx.doi.org/10.24266/0738-2898-22.1.41.
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Abstract Annual vinca (Catharanthus roseus) were grown in containers in a greenhouse and irrigated with a complete nutrient solution containing phosphite (0, 0.1, 0.3 mM), phosphate (0, 0.3, 0.5 mM), or combinations of these two compounds as a source of phosphorus. After 2 weeks, the plants were sprayed with a Phytophthora nicotianae zoospore inoculum to evaluate the potential for phosphite to protect annual vinca from Phytophthora shoot blight. To determine the extent and duration of protection from shoot blight provided by phosphite foliar applications, the plants were treated with phosphite foliar sprays (0.5 mM) at various intervals, and then inoculated. Application of phosphite to the soil/roots provided no protection from Phytophthora shoot blight. However, foliar applications of phosphite at a concentration of 0.5 mM at three to six day intervals gave protection similar to foliar applications of Aliette fungicide at 3 g/liter (2.5 lb/100 gal) applied at 14 day intervals.
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Chida, Toko, Masakatsu Ando, Tasuku Matsuki, Yutaro Masu, Yuko Nagaura, Teruko Takano-Yamamoto, Shinri Tamura, and Takayasu Kobayashi. "N-Myristoylation is essential for protein phosphatases PPM1A and PPM1B to dephosphorylate their physiological substrates in cells." Biochemical Journal 449, no. 3 (January 9, 2013): 741–49. http://dx.doi.org/10.1042/bj20121201.
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PPM [metal-dependent protein phosphatase, formerly called PP2C (protein phosphatase 2C)] family members play essential roles in regulating a variety of signalling pathways. While searching for protein phosphatase(s) that act on AMPK (AMP-activated protein kinase), we found that PPM1A and PPM1B are N-myristoylated and that this modification is essential for their ability to dephosphorylate the α subunit of AMPK (AMPKα) in cells. N-Myristoylation was also required for two other functions of PPM1A and PPM1B in cells. Although a non-myristoylated mutation (G2A) of PPM1A and PPM1B prevented membrane association, this relocalization did not likely cause the decreased activity towards AMPKα. In in vitro experiments, the G2A mutants exhibited reduced activities towards AMPKα, but much higher specific activity against an artificial substrate, PNPP (p-nitrophenyl phosphate), compared with the wild-type counterparts. Taken together, the results of the present study suggest that N-myristoylation of PPM1A and PPM1B plays a key role in recognition of their physiological substrates in cells.
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Yamaguchi, A., M. Fukushi, Y. Mizushima, Y. Shimizu, N. Takasugi, S. Arashima, and K. Ohyanagi. "Microassay for screening newborns for galactosemia with use of a fluorometric microplate reader." Clinical Chemistry 35, no. 9 (September 1, 1989): 1962–64. http://dx.doi.org/10.1093/clinchem/35.9.1962.
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Abstract We describe a microassay for measuring galactose (Gal) and galactose 1-phosphate (Gal-1-P) in dried blood spots. After a coupled enzyme reaction involving galactose dehydrogenase (GADH, EC 1.1.1.48) and alkaline phosphatase (AP, EC 3.1.3.1) in a microplate well, NADH fluorescence is measured by a highly sensitive fluorometric microplate reader, capable of rapid measurement of fluorescence (2 min per 96 samples). Within- and between-run CVs for measurements of Gal at 90 mg/L with Gal-1-P at 130 mg/L were both less than 5% (n = 8), and analytical recoveries for Gal at 90 mg/L and Gal-1-P at 130 mg/L were 98% and 92%, respectively. Five hundred dried blood-spot samples can be assayed within 2 h, with full calculation of results by an on-line microcomputer. This rapid and reliable assay system is very useful for the routine screening of newborns for galactosemia.
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Bro, Christoffer, Steen Knudsen, Birgitte Regenberg, Lisbeth Olsson, and Jens Nielsen. "Improvement of Galactose Uptake in Saccharomyces cerevisiae through Overexpression of Phosphoglucomutase: Example of Transcript Analysis as a Tool in Inverse Metabolic Engineering." Applied and Environmental Microbiology 71, no. 11 (November 2005): 6465–72. http://dx.doi.org/10.1128/aem.71.11.6465-6472.2005.
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ABSTRACT Through genome-wide transcript analysis of a reference strain and two recombinant Saccharomyces cerevisiae strains with different rates of galactose uptake, we obtained information about the global transcriptional response to metabolic engineering of the GAL gene regulatory network. One of the recombinant strains overexpressed the gene encoding the transcriptional activator Gal4, and in the other strain the genes encoding Gal80, Gal6, and Mig1, which are negative regulators of the GAL system, were deleted. Even though the galactose uptake rates were significantly different in the three strains, we surprisingly did not find any significant changes in the expression of the genes encoding the enzymes catalyzing the first steps of the pathway (i.e., the genes encoding Gal2, Gal1, Gal7, and Gal10). We did, however, find that PGM2, encoding the major isoenzyme of phosphoglucomutase, was slightly up-regulated in the two recombinant strains with higher galactose uptake rates. This indicated that PGM2 is a target for overexpression in terms of increasing the flux through the Leloir pathway, and through overexpression of PGM2 the galactose uptake rate could be increased by 70% compared to that of the reference strain. Based on our findings, we concluded that phosphoglucomutase plays a key role in controlling the flux through the Leloir pathway, probably due to increased conversion of glucose-1-phosphate to glucose-6-phosphate. This conclusion was supported by measurements of sugar phosphates, which showed that there were increased concentrations of glucose-6-phosphate, galactose-6-phosphate, and fructose-6-phosphate in the strain construct overexpressing PGM2.
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Kotake, Toshihisa, Daisuke Yamaguchi, Hiroshi Ohzono, Sachiko Hojo, Satoshi Kaneko, Hide-ki Ishida, and Yoichi Tsumuraya. "UDP-sugar Pyrophosphorylase with Broad Substrate Specificity Toward Various Monosaccharide 1-Phosphates from Pea Sprouts." Journal of Biological Chemistry 279, no. 44 (August 23, 2004): 45728–36. http://dx.doi.org/10.1074/jbc.m408716200.
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UDP-sugars, activated forms of monosaccharides, are synthesized throughde novoand salvage pathways and serve as substrates for the synthesis of polysaccharides, glycolipids, and glycoproteins in higher plants. A UDP-sugar pyrophosphorylase, designated PsUSP, was purified about 1,200-fold from pea (Pisum sativumL.) sprouts by conventional chromatography. The apparent molecular mass of the purified PsUSP was 67,000 Da. The enzyme catalyzed the formation of UDP-Glc, UDP-Gal, UDP-glucuronic acid, UDP-l-arabinose, and UDP-xylose from respective monosaccharide 1-phosphates in the presence of UTP as a co-substrate, indicating that the enzyme has broad substrate specificity toward monosaccharide 1-phosphates. Maximum activity of the enzyme occurred at pH 6.5–7.5, and at 45 °C in the presence of 2 mmMg2+. The apparentKmvalues for Glc 1-phosphate andl-arabinose 1-phosphate were 0.34 and 0.96 mm, respectively.PsUSPcDNA was cloned by reverse transcriptase-PCR.PsUSPappears to encode a protein with a molecular mass of 66,040 Da (600 amino acids) and possesses a uridine-binding site, which has also been found in a human UDP-N-acetylhexosamine pyrophosphorylase. Phylogenetic analysis revealed that PsUSP can be categorized in a group together with homologues fromArabidopsisand rice, which is distinct from the UDP-Glc and UDP-N-acetylhexosamine pyrophosphorylase groups. Recombinant PsUSP expressed inEscherichia colicatalyzed the formation of UDP-sugars from monosaccharide 1-phosphates and UTP with efficiency similar to that of the native enzyme. These results indicate that the enzyme is a novel type of UDP-sugar pyrophosphorylase, which catalyzes the formation of various UDP-sugars at the end of salvage pathways in higher plants.
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Tsakiris, Stylianos, Kyriakoula Marinou, and Kleopatra H. Schulpis. "The Effect of Galactose Metabolic Disorders on Rat Brain Na+,K+-ATPase Activity." Zeitschrift für Naturforschung C 57, no. 9-10 (October 1, 2002): 939–43. http://dx.doi.org/10.1515/znc-2002-9-1030.
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To evaluate the effect of galactose metabolic disorders on the brain Na+,K+-ATPase in suckling rats. Separate preincubations of various concentrations (1-16 mᴍ) of the compounds galactose-1-phosphate (Gal-1-P) and galactitol (galtol) with whole brain homogenates at 37 °C for 1 h resulted in a dose dependent inhibition of the enzyme whereas the pure enzyme (from porcine cerebral cortex) was stimulated. Glucose-1-phosphate (Glu-1-P) or galactose (Gal) stimulated both rat brain Na+,K+-ATPase and pure enzyme. A mixture of Gal-1-P (2 mm), galtol (2 mᴍ) and Gal (4 mᴍ), concentrations commonly found in untreated patients with classical galactosemia, caused a 35% (p < 0.001) rat brain enzyme inhibition. Additionally, incubation of a mixture of galtol (2 mᴍ) and Gal (1 mᴍ), which is usually observed in galactokinase deficient patients, resulted in a 25% (p < 0.001) brain enzyme inactivation. It is suggested that: a) The indirect inhibition of the brain Na+,K+-ATPase by Gal-1-P should be due to the presence of the epimer Gal and phosphate and that the pure enzyme direct activation by Gal-1-P and Glu-1-P to the presence of phosphate only. b) The observed brain Na+,K+-ATPase inhibitions in the presence of toxic concentrations of Gal-1-P and/ or galtol could modulate the neural excitability, the metabolic energy production and the catecholaminergic and serotoninergic system.
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Cui, Heng-Lin, Xia Gao, Xin Yang, and Xue-Wei Xu. "Halolamina pelagica gen. nov., sp. nov., a new member of the family Halobacteriaceae." International Journal of Systematic and Evolutionary Microbiology 61, no. 7 (July 1, 2011): 1617–21. http://dx.doi.org/10.1099/ijs.0.026799-0.
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Two extremely halophilic archaeal strains, TBN21T and TBN49, were isolated from the Taibei marine solar saltern near Lianyungang city, Jiangsu province, China. Cells of the two strains were pleomorphic and Gram-negative and colonies were red. Strains TBN21T and TBN49 were able to grow at 25–50 °C (optimum 37 °C), at 1.4–5.1 M NaCl (optimum 3.4–3.9 M) and at pH 5.5–9.5 (optimum pH 7.0–7.5) and neither strain required Mg2+ for growth. Cells lysed in distilled water and the minimal NaCl concentration to prevent cell lysis was 8 % (w/v). The major polar lipids of the two strains were phosphatidic acid, phosphatidylglycerol, phosphatidylglycerol phosphate methyl ester, phosphatidylglycerol sulfate and eight glycolipids; three of these glycolipids (GL3, GL4 and GL5) were chromatographically identical to sulfated mannosyl glucosyl diether (S-DGD-1), galactosyl mannosyl glucosyl diether (TGD-1) and mannosyl glucosyl diether (DGD-1), respectively. Phylogenetic analysis revealed that strains TBN21T and TBN49 formed a distinct clade with their closest relative, Halobaculum gomorrense JCM 9908T (89.0–89.5 % 16S rRNA gene sequence similarity). The DNA G+C contents of strains TBN21T and TBN49 were 64.8 and 62.7 mol%, respectively. DNA–DNA hybridization between strains TBN21T and TBN49 was 90.1 %. The phenotypic, chemotaxonomic and phylogenetic properties suggest that strains TBN21T and TBN49 represent a novel species in a new genus within the family Halobacteriaceae, for which the name Halolamina pelagica gen. nov., sp. nov. is proposed. The type strain of Halolamina pelagica is TBN21T ( = CGMCC 1.10329T = JCM 16809T).
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Jensen, Ulrich Glümer, Niels Jacob Brandt, Ernst Christensen, Flemming Skovby, Bent Nørgaard-Pedersen, and Henrik Simonsen. "Neonatal Screening for Galactosemia by Quantitative Analysis of Hexose Monophosphates Using Tandem Mass Spectrometry: A Retrospective Study." Clinical Chemistry 47, no. 8 (August 1, 2001): 1364–72. http://dx.doi.org/10.1093/clinchem/47.8.1364.
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Abstract Background: Classic galactosemia (OMIM 230400) is an inherited disorder in the metabolism of galactose caused by deficiency of the enzyme galactose 1-phosphate uridyl transferase (EC 2.7.7.12). Galactosemia leads to accumulation of galactose and galactose 1-phosphate (gal-1-P) in blood and tissues and, if untreated, produces neonatal death or severe mental retardation, cirrhosis of the liver, and cataracts. Hence, the disorder is included in many neonatal screening programs. Methods: We retrospectively analyzed filter-paper blood samples obtained 4–8 days postpartum for routine neonatal screening from 12 galactosemia patients and 2055 random controls. Total hexose monophosphates (HMPs) were used as a marker of gal-1-P and were assayed by negative-ion mode electrospray tandem mass spectrometry (tandem MS) with settings biased toward gal-1-P detection. The predominant precursor/product ion pair m/z 259/79 was used to quantify total HMPs by external standardization. Results: Linear calibration curves were obtained in the range 0–8 mmol/L gal-1-P. The detection limit was 0.1 mmol/L HMP, and total CVs ranged from 13% at the detection limit to <8% at >1 mmol/L HMP. The method was in agreement with an alkaline phosphatase-galactose dehydrogenase method. All samples from galactosemia patients contained increased HMP concentrations (range for patients, 2.6–5.2 mmol/L; range for reference group, <0.10–0.94 mmol/L). The diagnostic sensitivity and specificity were 100% at a cutoff of 1.2 mmol/L HMP. A Duarte/classic galactosemia compound heterozygous sample could be discriminated clearly from both patient and reference samples. Conclusion: Quantitative analysis of HMPs by tandem MS can be used in laboratory investigations of galactosemia.
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Alam, Md Kausar, and Susan G. W. Kaminskyj. "Aspergillus galactose metabolism is more complex than that of Saccharomyces: the story of GalDGAL7 and GalEGAL1." Botany 91, no. 7 (July 2013): 467–77. http://dx.doi.org/10.1139/cjb-2012-0270.
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Saccharomyces cerevisiae Hansen GAL1 (galactokinase) generates galactose-1-phosphate; GAL7 (galactose-1-phosphate uridylyltransferase) transfers UDP between galactose or glucose and their respective sugar-1-phosphate conjugates, and both are essential on galactose. Aspergillus nidulans ANID_04957 has 41% amino acid sequence identity with GAL1; ANID_06182 has 50% sequence identity with GAL7. The names Aspergillus nidulans GalE (galactokinase) and GalD (galactose-1-phosphate uridylyltransferase) are consistent with prior studies. Complemented galDΔ:ScGAL7 and galEΔ:ScGAL1 strains had wild-type phenotype, demonstrating functional homology. The galD5 and galE9 alleles were truncated. Strains galDΔ and galD5 were impaired on minimal medium containing 1% galactose (MM-Gal) at pH 7.5 and did not grow on MM-Gal pH 4.5. Strains galEΔ and galE9 grew on MM-Gal at both pH levels. Strains galDΔ and galEΔ produced wild-type conidiophores on minimal medium containing 1% glucose (MM-Glu) but few spores; for both, sporulation was lower on MM-Gal pH 7.5. GalD-GFP (green fluorescent protein) and GalE-GFP were cytosolic and upregulated on MM-Gal, consistent with quantitative real-time polymerase chain reaction. Galactofuranose immunolocalization in galDΔ resembled wild type on MM-Glu but was reduced on MM-Gal. The galEΔ strains had immunolocalizable Galf on all these media. Strains galDΔ and galEΔ were more sensitive to calcofluor, caspofungin, and itraconazole on MM-Gal. Neither galD nor galE is essential on galactose at high pH, implying additional routes for galactose metabolism in Aspergillus. Aspergillus galactose metabolism is more complex than that of S. cerevisiae.
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Neves, Ana R., Wietske A. Pool, Ana Solopova, Jan Kok, Helena Santos, and Oscar P. Kuipers. "Towards Enhanced Galactose Utilization by Lactococcus lactis." Applied and Environmental Microbiology 76, no. 21 (September 17, 2010): 7048–60. http://dx.doi.org/10.1128/aem.01195-10.
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ABSTRACT Accumulation of galactose in dairy products due to partial lactose fermentation by lactic acid bacteria yields poor-quality products and precludes their consumption by individuals suffering from galactosemia. This study aimed at extending our knowledge of galactose metabolism in Lactococcus lactis, with the final goal of tailoring strains for enhanced galactose consumption. We used directed genetically engineered strains to examine galactose utilization in strain NZ9000 via the chromosomal Leloir pathway (gal genes) or the plasmid-encoded tagatose 6-phosphate (Tag6P) pathway (lac genes). Galactokinase (GalK), but not galactose permease (GalP), is essential for growth on galactose. This finding led to the discovery of an alternative route, comprising a galactose phosphotransferase system (PTS) and a phosphatase, for galactose dissimilation in NZ9000. Introduction of the Tag6P pathway in a galPMK mutant restored the ability to metabolize galactose but did not sustain growth on this sugar. The latter strain was used to prove that lacFE, encoding the lactose PTS, is necessary for galactose metabolism, thus implicating this transporter in galactose uptake. Both PTS transporters have a low affinity for galactose, while GalP displays a high affinity for the sugar. Furthermore, the GalP/Leloir route supported the highest galactose consumption rate. To further increase this rate, we overexpressed galPMKT, but this led to a substantial accumulation of α-galactose 1-phosphate and α-glucose 1-phosphate, pointing to a bottleneck at the level of α-phosphoglucomutase. Overexpression of a gene encoding α-phosphoglucomutase alone or in combination with gal genes yielded strains with galactose consumption rates enhanced up to 50% relative to that of NZ9000. Approaches to further improve galactose metabolism are discussed.
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Clark, Mary C., Mabel Pang, Daniel K. Hsu, Fu-Tong Liu, Sven de Vos, Randy D. Gascoyne, Jonathan Said, and Linda G. Baum. "Galectin-3 binds to CD45 on diffuse large B-cell lymphoma cells to regulate susceptibility to cell death." Blood 120, no. 23 (November 29, 2012): 4635–44. http://dx.doi.org/10.1182/blood-2012-06-438234.
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Abstract Diffuse large B-cell lymphoma (DLBCL) is the most common non-Hodgkin lymphoma and an aggressive malignancy. Galectin-3 (gal-3), the only antiapoptotic member of the galectin family, is overexpressed in DLBCL. While gal-3 can localize to intracellular sites, gal-3 is secreted by DLBCL cells and binds back to the cell surface in a carbohydrate-dependent manner. The major counterreceptor for gal-3 on DLBCL cells was identified as the transmembrane tyrosine phosphatase CD45. Removal of cell-surface gal-3 from CD45 with the polyvalent glycan inhibitor GCS-100 rendered DLBCL cells susceptible to chemotherapeutic agents. Binding of gal-3 to CD45 modulated tyrosine phosphatase activity; removal of endogenous cell-surface gal-3 from CD45 with GCS-100 increased phosphatase activity, while addition of exogenous gal-3 reduced phosphatase activity. Moreover, the increased susceptibility of DLBCL cells to chemotherapeutic agents after removal of gal-3 by GCS-100 required CD45 phosphatase activity. Gal-3 binding to a subset of highly glycosylated CD45 glycoforms was regulated by the C2GnT-1 glycosyltransferase, indicating that specific glycosylation of CD45 is important for regulation of gal-3–mediated signaling. These data identify a novel role for cell-surface gal-3 and CD45 in DLBCL survival and suggest novel therapeutic targets to sensitize DLBCL cells to death.
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Tsakiris, Stylianos, and Kleopatra H. Schulpis. "The Effect of Galactose Metabolic Disorders on Rat Brain Acetylcholinesterase Activity." Zeitschrift für Naturforschung C 55, no. 9-10 (October 1, 2000): 852–56. http://dx.doi.org/10.1515/znc-2000-9-1032.
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Abstract To evaluate whether in classical galactosemia galactose (Gal), galactose-1-phosphate (Gal-1-P) and galactitol (Galtol) affect brain acetylcholinesterase (AChE) activity, various concentrations (1-16 mм) of these compounds were preincubated with brain homogenates of suckling rats as well as with pure eel Electroforus electricus AChE at 37 °C for 1 h. Initially, Galtol (up to 2.0 mм) increased (25%) AChE activity which decreased, thereafter, reaching the control value in high Galtol concentrations. Gal-1-P decreased gradually the enzyme activity reaching a plateau (38%), when incubated with 8-16 mM. However, when the usually found 2 mм of Galtol and 2 mм of Gal-1-P. concentrations in galactosemia were added in the incubation mixture simultaneously, brain AChE was stimulated (16%). Galtol or Gal-1-P modulated brain AChE as well as enzyme activity of E.electricus in the same way. Gal, Glucose (Glu) and glucose-1-phosphate (Glu-1-P) had no effect on AChE activity. It is suggested that Galtol as well as Gal-1-P can affect acetylcholine degradation acting directly on AChE molecule. Consequently the direct action of these substances on the enzyme might explain the brain cholinergic dysfunction in untreated galactosemia patients.