Journal articles: 'Blood proteins Physiology'

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Davies, Peter L., Choy L. Hew, and Garth L. Fletcher. "Fish antifreeze proteins: physiology and evolutionary biology." Canadian Journal of Zoology 66, no. 12 (December 1, 1988): 2611–17. http://dx.doi.org/10.1139/z88-385.

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Many marine teleosts have adapted to ice-laden seawater by evolving antifreeze proteins and glycoproteins. These proteins are synthesized in the liver for export to the blood where they circulate at levels of up to 20 mg/mL. There are at least four distinct antifreeze protein classes differing in carbohydrate content, amino acid composition, protein sequence, and secondary structure. In addition to antifreeze structural diversity, fish species differ considerably with respect to mechanisms controlling seasonal regulation of plasma antifreeze concentrations. Some species synthesize antifreeze proteins immediately before the onset of freezing conditions, some synthesize them in response to such conditions, whereas others possess high concentrations all year. Endogenous rhythms, water temperature, photoperiod, and pituitary hormones have all been implicated as regulators of plasma antifreeze protein levels. The structural diversity of antifreeze proteins and their occurrence in a wide range of fish species suggest that they evolved separately and recently during Cenozoic glaciation. Invariably, the genes coding for these antifreeze proteins are amplified, sometimes as long tandem arrays, suggesting intense selective pressure to produce large amounts of protein. The distribution of antifreeze gene types among fish species suggests that they could serve as important tools for studying phylogenetic relationships.

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Jia, Ruizhe, Jingyun Li, Can Rui, Hui Ji, Hongjuan Ding, Yuanqing Lu, Wei De, and Lizhou Sun. "Comparative Proteomic Profile of the Human Umbilical Cord Blood Exosomes between Normal and Preeclampsia Pregnancies with High-Resolution Mass Spectrometry." Cellular Physiology and Biochemistry 36, no. 6 (2015): 2299–306. http://dx.doi.org/10.1159/000430193.

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Background/Aims: Exosomes are extracellular vesicles that are involved in several biological processes. The roles of proteins from human umbilical cord blood exosomes in the pathogenesis of preeclampsia remains poorly understood. Methods: In this study, we used high-resolution LC-MS/MS technologies to construct a comparative proteomic profiling of human umbilical cord blood exosomes between normal and preeclamptic pregnancies. Results: A total of 221 proteins were detected in human umbilical cord blood exosomes, with 14 upregulated and 15 downregulated proteins were definitively identified between preeclamptic and control pregnancies. Further bioinformatics analysis (Gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analysis) indicated that these differentially expressed proteins correlate with enzyme regulator activity, binding, extracellular region, cell part, biological regulation, cellular process and complement and coagulation cascades occurring during pathological changes of preeclampsia. Conclusion: Our results show significantly altered expression profiles of proteins in human umbilical cord blood exosomes between normal and preeclampsia pregnancies. These proteins may be involved in the etiology of preeclampsia.

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Croxatto, HR. "How Many Peptidic Hormones Can Derive From Blood Plasma Proteins?" Physiology 5, no. 5 (October 1, 1990): 201–4. http://dx.doi.org/10.1152/physiologyonline.1990.5.5.201.

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Peptides having structures identical or related to some already known hormones have been obtained using pepsin as a hydrolytic agent acting at acid pH upon plasma substrates. The data suggest the existence of systems similar to renin-angiotensin for the generation of active peptides other than angiotensin or kinins.

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Ohno, H., K. Yamashita, R. Doi, K. Yamamura, T. Kondo, and N. Taniguchi. "Exercise-induced changes in blood zinc and related proteins in humans." Journal of Applied Physiology 58, no. 5 (May 1, 1985): 1453–58. http://dx.doi.org/10.1152/jappl.1985.58.5.1453.

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Effects of cycle ergometer exercise (approximately 75% maximum ventilatory O2 consumption for 30 min) on the concentrations of zinc and related proteins in erythrocytes and/or plasma were studied on 11 sedentary male students. Lower concentrations of total zinc and of zinc derived from carbonic anhydrase I type (CA-I) in erythrocytes were observed immediately after exercise, but they disappeared after 30 min of rest. The change in total zinc concentration in erythrocytes correlated well with that in CA-I concentration immediately after exercise, as well as after rest. The concentration of carbonic anhydrase II type (CA-II)-derived zinc did not vary substantially at any time. On the other hand, there were significant increases in the plasma concentrations of total zinc and of alpha 2-macroglobulin (alpha 2-MG)-bound zinc immediately after exercise, whereas no such effect was noted in albumin-bound zinc. A positive correlation was found between total zinc and alpha 2-MG concentrations in plasma immediately after exercise. In addition, the change in the activity of alkaline phosphatase, a zinc metalloenzyme, correlated well with that in the total zinc concentration in plasma. These results suggest that a brief physical exercise induces the movement of zinc into plasma.

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Teahan, Carmel G., Hugh A. McKenzie, and Mervyn Griffiths. "Some monotreme milk “whey” and blood proteins." Comparative Biochemistry and Physiology Part B: Comparative Biochemistry 99, no. 1 (January 1991): 99–118. http://dx.doi.org/10.1016/0305-0491(91)90014-5.

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Richardson, Samantha J., Julie A. Monk, Caroline A. Shepherdley, Lars O. E. Ebbesson, Frank Sin, Deborah M. Power, Peter B. Frappell, Josef Köhrle, and Marilyn B. Renfree. "Developmentally regulated thyroid hormone distributor proteins in marsupials, a reptile, and fish." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 5 (May 2005): R1264—R1272. http://dx.doi.org/10.1152/ajpregu.00793.2004.

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Thyroid hormones are essential for vertebrate development. There is a characteristic rise in thyroid hormone levels in blood during critical periods of thyroid hormone-regulated development. Thyroid hormones are lipophilic compounds, which readily partition from an aqueous environment into a lipid environment. Thyroid hormone distributor proteins are required to ensure adequate distribution of thyroid hormones, throughout the aqueous environment of the blood, and to counteract the avid partitioning of thyroid hormones into the lipid environment of cell membranes. In human blood, these proteins are albumin, transthyretin and thyroxine-binding globulin. We analyzed the developmental profile of thyroid hormone distributor proteins in serum from a representative of each order of marsupials ( M. eugenii; S.crassicaudata), a reptile ( C. porosus), in two species of salmonoid fishes ( S. salar; O. tshawytsch), and throughout a calendar year for sea bream ( S. aurata). We demonstrated that during development, these animals have a thyroid hormone distributor protein present in their blood which is not present in the adult blood. At least in mammals, this additional protein has higher affinity for thyroid hormones than the thyroid hormone distributor proteins in the blood of the adult. In fish, reptile and polyprotodont marsupial, this protein was transthyretin. In a diprotodont marsupial, it was thyroxine-binding globulin. We propose an hypothesis that an augmented thyroid hormone distributor protein network contributes to the rise in total thyroid hormone levels in the blood during development.

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Synelnyk, T. B., O. O. Kravchenko, O. S. Kostiuk, O. M. Savchuk, S. A. Sukhodolia, and L. I. Ostapchenko. "DISTRIBUTION OF SERINE PROTEASES IN BLOOD PLASMA AND PANCREAS IN CHRONIC PANCREATITIS AND ONCOPATHOLOGY." Fiziolohichnyĭ zhurnal 68, no. 6 (December 8, 2022): 31–43. http://dx.doi.org/10.15407/fz68.06.031.

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The aim of our study was to evaluate the trypsin-like serine proteases (TLPs) distribution between systemic circulation and pancreatic tissue and to investigate the peculiarities of their involvement in the extracellular matrix components degradation in patients with pancreatic pathologies with electrophoretic analysis methods using. Тhe Khmelnitsky Regional Clinical Hospital patients aged 28-89 were selected for this study: 20 people with chronic pancreatitis (group CP); 20 people with pancreatic cancer (group PC); 20 conditionally healthy persons (control). Blood plasma samples and pancreatic tissue homogenates were obtained from all the patients, from which the TLPs fractions were subsequently obtained by the affinity chromatography method. The study showed that TLPs content in the blood plasma of patients with pancreatic pathologies is higher, and in tissue homogenates is lower relative to the values of the corresponding indicators in the control. Disk-electrophoresis using showed that TLPs fractions obtained from the blood plasma of patients of all studied groups contain a lot of high molecular weight (HMW) proteins, while TLPs from the pancreatic tissue homogenates of patients with pancreatic pathologies mainly consists of low molecular weight (LMW) proteins. Enzyme-electrophoresis results showed that all TLPs fractions include enzymes with fibrinogenolytic, gelatinolytic and collagenolytic activity. In plasma, the first were represented by medium molecular weight (MMW) proteins, and the last two groups included a lot of HMW proteins as well as proteins with very high molecular weight. In homogenates, fibrinogenolytic activity was characteristic for LMW proteins only, whereas gelatinases and collagenases were represented by both MMW and LMW proteins. Our results indicate the differences in the TLPs fractions components obtained from blood plasma and pancreatic tissue of patients with investigated pathologies, as well as significant distinctions in the processes of extracellular matrix remodeling under СР and РС.

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Lampe, L., K. Wienhold, G. Meyer, F. Baisch, H. Maass, W. Hollmann, and R. Rost. "Effects of simulated microgravity (HDT) on blood fluidity." Journal of Applied Physiology 73, no. 4 (October 1, 1992): 1366–69. http://dx.doi.org/10.1152/jappl.1992.73.4.1366.

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Exposures to microgravity and head-down tilt (HDT) produce similar changes in body fluid. This causes an increase in hematocrit that significantly affects hemorheological values. Lack of physical stimulation under bed rest conditions and the relative immobility of the crew during spaceflight also affects the blood fluidity. A group of six healthy male subjects participated as volunteers, and blood samples were collected 10 days before, on day 2 and day 9, and 2 days after the HDT phase. Blood rheology was quantified by plasma viscometry, red cell aggregability, and red cell deformability. A reduced red cell deformability, an indication of the diminished quality of the red blood cells, was measured under HDT conditions that finally led to the so-called “space flight anemia.” Enhanced red cell membrane fragility induced by diminished physical activity and an increase in hemoglobin concentration are responsible for this effect. Plasma viscosity is reduced as a result of diminished plasma proteins. However, despite the reduction in plasma proteins, including fibrinogen, alpha 2-macroglobulin, and immunoglobulin M, red cell aggregation was enhanced, principally because of the increase in hematocrit. Our results of hemorheological alterations under HDT conditions may help to elucidate the formerly documented hematologic changes during spaceflight.

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Martino, Tami A., Nazneen Tata, Georg A. Bjarnason, Marty Straume, and Michael J. Sole. "Diurnal protein expression in blood revealed by high throughput mass spectrometry proteomics and implications for translational medicine and body time of day." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 3 (September 2007): R1430—R1437. http://dx.doi.org/10.1152/ajpregu.00183.2007.

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Molecular gene cycling is useful for determining body time of day (BTOD) with important applications in personalized medicine, including cardiovascular disease and cancer, our leading causes of death. However, it impractically requires repetitive invasive tissue sampling that is obviously not applicable for humans. Here we characterize diurnal protein cycling in blood using high-throughput proteomics; blood proteins are easily accessible, minimally invasive, and can importantly serve as surrogates for what is happening elsewhere in the body in health and disease. As proof of the concept, we used normal C57BL/6 mice maintained under regular 24-h light and dark cycles. First, we demonstrated fingerprint patterns in 24-h plasma, revealed using surface-enhanced laser desorption and ionization (SELDI). Second, we characterized diurnal cycling proteins in blood using chromatography and tandem electrospray ionization mass spectrometry. Importantly, we noted little association between the cycling blood proteome and tissue transcriptome, delineating the necessity to identify de novo cycling proteins in blood for measuring BTOD. Furthermore, we explored known interaction networks to identify putative functional pathways regulating protein expression patterns in blood, thus shedding new light on our understanding of integrative physiology. These studies have profound clinical significance in translating the concept of BTOD to the practical realm for molecular diagnostics and open new opportunities for clinically relevant discoveries when applied to ELISA-based molecular testing and/or point-of-care devices.

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van de Graaf, Stan F. J., Joost G. J. Hoenderop, and René J. M. Bindels. "Regulation of TRPV5 and TRPV6 by associated proteins." American Journal of Physiology-Renal Physiology 290, no. 6 (June 2006): F1295—F1302. http://dx.doi.org/10.1152/ajprenal.00443.2005.

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The epithelial Ca2+ channels TRPV5 and TRPV6 are the most Ca2+-selective members of the TRP channel superfamily. These channels are the prime target for hormonal control of the active Ca2+ flux from the urine space or intestinal lumen to the blood compartment. Insight into their regulation is, therefore, pivotal in our understanding of the (patho)physiology of Ca2+ homeostasis. The recent elucidation of TRPV5/6-associated proteins has provided new insight into the molecular mechanisms underlying the regulation of these channels. In this review, we describe the various means of TRPV5/6 regulation, the role of channel-associated proteins herein, and the relationship between both processes.

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Rossing, T. H., N. Maffeo, and V. Fencl. "Acid-base effects of altering plasma protein concentration in human blood in vitro." Journal of Applied Physiology 61, no. 6 (December 1, 1986): 2260–65. http://dx.doi.org/10.1152/jappl.1986.61.6.2260.

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We altered the concentration of plasma proteins in human blood in vitro by adding solutions with [Na+], [K+], and [Cl-] resembling those in normal blood plasma, either protein-free or with a high concentration of human albumin. After equilibrating the samples with a gas containing 5% CO2-12% O2–83% N2 at 37 degrees C, we measured pH, PCO2, and PO2; in separated plasma, we determined the concentrations of total plasma proteins and albumin and of the completely dissociated electrolytes (strong cations Na+, K+, Mg2+ and anions Cl-, citrate3-). With PCO2 nearly constant (mean = 35.5 Torr; coefficient of variation = 0.02), lowering plasma protein concentration produced a metabolic alkalosis, whereas increasing plasma albumin concentration gave rise to a metabolic acidosis. These acid-base disturbances occurred independently of a minor variation in the balance between the sums of strong cations and anions. We quantified the dependence of several acid-base variables in plasma on albumin (or total protein) concentration. Normal plasma proteins are weak nonvolatile acids. Although their concentration is not regulated as part of acid-base homeostasis, hypoproteinemia and hyperalbuminemia per se produce alkalosis and acidosis, respectively.

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12

Persu, Alexandre. "G proteins: fine tuning of blood pressure regulation." Journal of Hypertension 23, no. 8 (August 2005): 1465–67. http://dx.doi.org/10.1097/01.hjh.0000174610.72145.76.

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Hom, Sharon, Melissa A. Fleegal, Richard D. Egleton, Christopher R. Campos, Brian T. Hawkins, and Thomas P. Davis. "Comparative changes in the blood-brain barrier and cerebral infarction of SHR and WKY rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 5 (May 2007): R1881—R1892. http://dx.doi.org/10.1152/ajpregu.00761.2005.

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Hypertension is involved in the exacerbation of stroke. It is unclear how blood-brain barrier (BBB) tight-junction (TJ) and ion transporter proteins critical for maintaining brain homeostasis contribute to cerebral infarction during hypertension development. In the present study, we investigated cerebral infarct volume following permanent 4-h middle cerebral artery occlusion (MCAO) and characterized the expression of BBB TJ and ion transporter proteins in brain microvessels of spontaneously hypertensive rats (SHR) compared with age-matched Wistar-Kyoto (WKY) rats at 5 wk (prehypertension), 10 wk (early-stage hypertension), and 15 wk (later-stage hypertension) of age. Hypertensive SHR show increased infarct volume following MCAO compared with WKY control rats. BBB TJ and ion transporter proteins, known to contribute to edema and fluid volume changes in the brain, show differential protein expression patterns during hypertension development. Western blot analysis of TJ protein zonula occludens-2 (ZO-2) showed decreased expression, while ion transporter, Na+/H+ exchanger 1 (NHE-1), was markedly increased in hypertensive SHR. Expression of TJ proteins ZO-1, occludin, actin, claudin-5, and Na+-K+-2Cl− cotransporter remain unaffected in SHR compared with control. Selective inhibition of NHE-1 using dimethylamiloride significantly attenuated ischemia-induced infarct volume in hypertensive SHR following MCAO, suggesting a novel role for NHE-1 in the brain in the regulation of ischemia-induced infarct volume in SHR.

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Rubinsky, B., M. Mattioli, A. Arav, B. Barboni, and G. L. Fletcher. "Inhibition of Ca2+ and K+ currents by "antifreeze" proteins." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 262, no. 3 (March 1, 1992): R542—R545. http://dx.doi.org/10.1152/ajpregu.1992.262.3.r542.

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For the last two decades, the research on fish “antifreeze” proteins has focused exclusively on their ability to depress noncolligatively blood plasma freezing points, presumably by binding to ice crystals. We report evidence that antifreeze polypeptides from the winter flounder (Pseudopleuronectes americanus) have another special property, the ability to block ion channels. In experiments with porcine granulosa cells we show, using the patch-clamp technique in the whole cell configuration, that these proteins suppress effectively calcium and potassium currents. The results of dose-response studies indicate a protein-protein interaction mechanism.

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Pastushkova, L. Kh, A. G. Goncharova, G. Yu Vasilyeva, S. K. Tagirova, D. N. Kashirina, O. V. Sayk, J. Rittweger, and I. M. Larina. "Search for Blood Proteome Proteins Involved in the Regulation of Bone Remodeling in Astronauts." Human Physiology 45, no. 5 (September 2019): 536–42. http://dx.doi.org/10.1134/s0362119719050128.

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Kucherenko, Yuliya V., and Ingolf Bernhardt. "Natural Antioxidants Improve Red Blood Cell “Survival” in Non-Leukoreduced Blood Samples." Cellular Physiology and Biochemistry 35, no. 5 (2015): 2055–68. http://dx.doi.org/10.1159/000374012.

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Background: Blood collected in an anticoagulant can be kept refrigerated in an unmodified state within 5 - 6 weeks. Oxidative damage is considered to be a one of the major factors contributing to the development of storage lesions. Lipid and membrane proteins oxidation results in changes in cation gradients that affect the cell survival. Aim: In the present study we used the natural antioxidants and ion channels blockers (L-carnosine, spermine, phloretin and their mixtures) to prolong “survival” of red blood cells (RBCs), measured as the lack of PS exposure and cell hemolysis, in the Alsever's preservative solution upon hypothermic storage. Results: We show that the mixture of carnosine (20 mM), spermine (20 µM) and phloretin (100 µM) effectively blunted phosphatidylserine (PS) exposure, Ca2+ accumulation and RBCs hemolysis in non-leukoreduced low (∼2%) hematocrit samples after 36 days of storage as well as after 1 day of post-storage incubation of the stored cells in physiological saline solution. In addition, a slight but significant decrease in PS exposure was observed in non-leukoreduced high (∼20%) hematocrit samples after 36 days of storage with the mixture of substances. Conclusion: We conclude that the use of the mixture of natural antioxidants (carnosine, spermine, and phloretin) as an additive to blood preservative solution provides better RBCs storage and “survival”.

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Klyuyev, D. A., L. E. Muravlyova, and V. B. Molotov-Luchanskiy. "Oxidized proteins in blood cells of patients with chronic kidney disease." Free Radical Biology and Medicine 65 (September 2013): S35. http://dx.doi.org/10.1016/j.freeradbiomed.2013.08.043.

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Muravlyova, Larissa, Vilen Molotov-Luchanskiy, Ryszhan Bakirova, Dmitriy Klyuvev, Ludmila Demidchik, Dinara Omertayeva, Valentina Lee, and Irina Beinikova. "Oxidazed proteins in blood of patients with nephropathies of various origins." Free Radical Biology and Medicine 120 (May 2018): S53. http://dx.doi.org/10.1016/j.freeradbiomed.2018.04.174.

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Koos, Robert D. "Minireview: Putting Physiology Back into Estrogens' Mechanism of Action." Endocrinology 152, no. 12 (September 27, 2011): 4481–88. http://dx.doi.org/10.1210/en.2011-1449.

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After decades of research, the mechanism by which estrogens stimulate the proliferation of epithelial cells in the endometrium and mammary gland, and in the carcinomas that arise in those tissues, is still not understood. Cells do not proliferate in response to 17β-estradiol (E2) alone, and although it is widely recognized that growth factors play a role in E2's proliferative effect, exactly how they are involved is unclear. It has long been known that the proliferation of endometrial epithelial cells is preceded by dramatic increases in blood flow and microvascular permeability, filling the subepithelial stroma with plasma and the proteins it contains, such as IGF-I, which is known to synergize with E2 in the induction of cell proliferation. The hyperpermeability is caused by vascular endothelial growth factor (VEGF), which is rapidly induced by E2, via the transcription factors hypoxia-inducible factor 1 and estrogen receptor α, in luminal epithelial cells in vivo. As we recently showed, VEGF is also strongly induced in endometrial cancer cells in vitro when excessive degradation of hypoxia-inducible factor 1α, caused by the abnormally high oxygen level to which cultured cells are exposed, is prevented. Putting these facts together, we now propose a new model of E2-induced proliferation in which VEGF-induced vascular hyperpermeability plays an essential role. E2 first induces the expression by endometrial epithelial cells of VEGF, which then acts in a paracrine manner to induce interendothelial cell gaps in subepithelial blood vessels, through which plasma and the proteins therein enter the adjacent stroma. Plasma carries even more E2, which circulates bound to proteins, and IGF-l, which together drive epithelial cells completely through the cell cycle.

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Ratych, I. B. "Petro Lahodyuk — Doctor of Biological Sciences, Professor, Academician of the National Academy of Agrarian Sciences of Ukraine, Honourable Man of Science and Technology of Ukraine (1924–1994)." Animal Biology 22, no. 3 (September 2020): 8–10. http://dx.doi.org/10.15407/animbiol22.03.008.

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Petro Lahodyuk is the Doctor of Biological Sciences, professor, Academician of NAAS, Honourable Man of Science and Technology of Ukraine. Academician Lahodyuk was a leading researcher of animal lactation physiology. He contributed greatly into research on fraction composition and antigene properties of soluble proteins in mammary gland of open heifers, heifers and lactating cows, open and pregnant cows, compared their immune and chemical properties with milk and blood serum proteins, researched amino acidic and peptoid content of albumins in mammary gland tissues and blood serum of open heifers, heifers and cows, established the role of alveolar epithelium, excretory ducts and milk ducts in creating milk serum proteins, studied the role of a number of hormones in milk formation processes regulation, in particular regulation of milk and blood serum protein biosynthesis.

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Ouali, Radouane, Larissa Rezende Vieira, Didier Salmon, and Sabrina Bousbata. "Early Post-Prandial Regulation of Protein Expression in the Midgut of Chagas Disease Vector Rhodnius prolixus Highlights New Potential Targets for Vector Control Strategy." Microorganisms 9, no. 4 (April 11, 2021): 804. http://dx.doi.org/10.3390/microorganisms9040804.

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Chagas disease is a vector-borne parasitic disease caused by the flagellated protozoan Trypanosoma cruzi and transmitted to humans by a large group of bloodsucking triatomine bugs. Triatomine insects, such as Rhodnius prolixus, ingest a huge amount of blood in a single meal. Their midgut represents an important interface for triatomine–trypanosome interactions. Furthermore, the development of parasites and their vectorial transmission are closely linked to the blood feeding and digestion; thus, an understanding of their physiology is essential for the development of new strategies to control triatomines. In this study, we used label-free quantitative proteomics to identify and analyze the early effect of blood feeding on protein expression in the midgut of Rhodnius prolixus. We both identified and quantified 124 proteins in the anterior midgut (AM) and 40 in the posterior midgut (PM), which vary significantly 6 h after feeding. The detailed analysis of these proteins revealed their predominant involvement in the primary function of hematophagy, including proteases, proteases inhibitors, amino acids metabolism, primary metabolites processing, and protein folding. Interestingly, our proteomics data show a potential role of the AM in protein digestion. Moreover, proteins related to detoxification processes and innate immunity, which are largely accepted to be triggered by blood ingestion, were mildly modulated. Surprisingly, one third of blood-regulated proteins in the AM have unknown function. This work contributes to the improvement of knowledge on the digestive physiology of triatomines in the early hours post-feeding. It provides key information for selecting new putative targets for the development of triatomine control tools and their potential role in the vector competence, which could be applied to other vector species.

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Ohanyan, Vahagn, Sean M. Raph, Marc M. Dwenger, Xuemei Hu, Thomas Pucci, Gregory Mack, Joseph B. Moore, William M. Chilian, Aruni Bhatnagar, and Matthew A. Nystoriak. "Myocardial Blood Flow Control by Oxygen Sensing Vascular Kvβ Proteins." Circulation Research 128, no. 6 (March 19, 2021): 738–51. http://dx.doi.org/10.1161/circresaha.120.317715.

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Rationale: Voltage-gated potassium (Kv) channels in vascular smooth muscle are essential for coupling myocardial blood flow (MBF) with the metabolic demand of the heart. These channels consist of a transmembrane pore domain that associates with auxiliary Kvβ (voltage-gated potassium channel β)1 and Kvβ2 proteins, which differentially regulate Kv function in excitable cells. Nonetheless, the physiological role of Kvβ proteins in regulating vascular tone and metabolic hyperemia in the heart remains unknown. Objective: To test the hypothesis that Kvβ proteins confer oxygen sensitivity to vascular tone and are required for regulating blood flow in the heart. Methods and Results: Mice lacking Kvβ2 subunits exhibited suppressed MBF, impaired cardiac contractile performance, and failed to maintain elevated arterial blood pressure in response to catecholamine-induced stress. In contrast, ablation of Kvβ1.1 reduced cardiac workload, modestly elevated MBF, and preserved cardiac function during stress compared with wild-type mice. Coronary arteries isolated from Kvβ2 −/− , but not Kvβ1.1 −/− , mice had severely blunted vasodilation to hypoxia when compared with arteries from wild-type mice. Moreover, vasodilation of small diameter coronary and mesenteric arteries due to L-lactate, a biochemical marker of reduced tissue oxygenation and anaerobic metabolism, was significantly attenuated in vessels isolated from Kvβ2 −/− mice. Inducible enhancement of the Kvβ1:Kvβ2 ratio in Kv1 channels of arterial smooth muscle abolished L-lactate-induced vasodilation and suppressed the relationship between MBF and cardiac workload. Conclusions: The Kvβ proteins differentially regulate vascular tone and MBF, whereby Kvβ2 promotes, and Kvβ1.1 inhibits oxygen-dependent vasodilation and augments blood flow upon heightened metabolic demand.

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Santamaria, Salvatore, and Rens de Groot. "ADAMTS proteases in cardiovascular physiology and disease." Open Biology 10, no. 12 (December 2020): 200333. http://dx.doi.org/10.1098/rsob.200333.

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The a disintegrin-like and metalloproteinase with thrombospondin motif (ADAMTS) family comprises 19 proteases that regulate the structure and function of extracellular proteins in the extracellular matrix and blood. The best characterized cardiovascular role is that of ADAMTS-13 in blood. Moderately low ADAMTS-13 levels increase the risk of ischeamic stroke and very low levels (less than 10%) can cause thrombotic thrombocytopenic purpura (TTP). Recombinant ADAMTS-13 is currently in clinical trials for treatment of TTP. Recently, new cardiovascular roles for ADAMTS proteases have been discovered. Several ADAMTS family members are important in the development of blood vessels and the heart, especially the valves. A number of studies have also investigated the potential role of ADAMTS-1, -4 and -5 in cardiovascular disease. They cleave proteoglycans such as versican, which represent major structural components of the arteries. ADAMTS-7 and -8 are attracting considerable interest owing to their implication in atherosclerosis and pulmonary arterial hypertension, respectively. Mutations in the ADAMTS19 gene cause progressive heart valve disease and missense variants in ADAMTS6 are associated with cardiac conduction. In this review, we discuss in detail the evidence for these and other cardiovascular roles of ADAMTS family members, their proteolytic substrates and the potential molecular mechanisms involved.

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Manns, J. G., and P. J. Lewing. "Protein production by sheep embryos during the period of maternal recognition of pregnancy." Canadian Journal of Physiology and Pharmacology 64, no. 9 (September 1, 1986): 1223–28. http://dx.doi.org/10.1139/y86-207.

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An embryo must be present in the uterus 12–13 days after estrus to prevent regression of the ovine corpus luteum. The present experiments were designed to determine if embryo-specific secretory proteins could be detected in the maternal blood at the time of maternal recognition of pregnancy. In two experiments, 92 embryos were flushed from 47 ewes at 14–15 days after estrus. Embryos were incubated in vitro for 24 h and the proteins in the media were harvested. Antisera to proteins in both flushing and incubation medium were produced in rabbits. In experiment 1, crude fractions were used for antibody production and radioimmunoassays were established for protein peaks separated on a 1.1 × 75 cm G-100 Sephadex column. Two low molecular weight fractions (EPiv and EPv) appeared to be embryo specific but were not detectable in jugular vein sera of 14- to 15-day pregnant animals. In experiment 2, proteins derived from uterine flushes and from embryo incubations were chromatographed on a 2.5 × 85 cm column of G-100 Sephadex. The protein peaks were measured, pooled, lyophilized, and used for immunization of rabbits. As in experiment 1, antisera were generated, some of which seemed to be directed against embryo-specific proteins. However, we could not detect these fractions in the uterine vein blood of pregnant animals. Thus, embryo-specific proteins are either confined to the uterus or they appear in the blood in quantities that are undetectable with our assay system.

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Kobayashi, T., K. Nitta, R. Takahashi, K. Kurashima, B. Robertson, and Y. Suzuki. "Activity of pulmonary surfactant after blocking the associated proteins SP-A and SP-B." Journal of Applied Physiology 71, no. 2 (August 1, 1991): 530–36. http://dx.doi.org/10.1152/jappl.1991.71.2.530.

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This study investigated the role of sympathetic withdrawal on blood flow responses in cutaneous arteriovenous anastomoses (AVAs) and capillaries to direct and indirect heat stress. This was achieved by clamping sympathetic activity (SC) to the tail of anesthetized rats so that constrictor tone remained invariant during exposure of either the animal's tail (direct heating) or body (indirect heating) to a 35 degrees C environment. Flow through the AVAs in the tail was evaluated by laser-Doppler flowmetry (LDF), while capillary flow was investigated by videodensitometry measurements of blood cell velocity (CBV) in single capillaries within the subepidermal vascular plexus. Both direct and indirect heating significantly increased LDF and CBV. In comparison to blood flow responses in sham-operated control rats, the SC procedure resulted in significantly lower LDF responses to both direct and indirect heat stress. By contrast, the response of CBV was not significantly affected by SC during either mode of heating. These results indicate that the withdrawal of sympathetic constrictor tone plays a role in the response of cutaneous AVAs, but not precapillary arterioles, to direct as well as indirect heat stress. Additional studies on unanesthetized animals showed that superimposing body heating on a base of local heating elicited a further increase in LDF, suggesting that local heating does not deplete neural mediated dilatory reserve.

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Saari, Jack T. "Copper deficiency and cardiovascular disease: role of peroxidation, glycation, and nitration." Canadian Journal of Physiology and Pharmacology 78, no. 10 (October 1, 2000): 848–55. http://dx.doi.org/10.1139/y00-054.

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Dietary copper deficiency causes a variety of cardiovascular deficits. Systemic effects include high blood pressure, enhancement of inflammation, anemia, reduced blood clotting, and possibly arteriosclerosis. Effects on specific organs or tissues include weakened structural integrity of the heart and blood vessels, impairment of energy use by the heart, reduced ability of the heart to contract, altered ability of blood vessels to control their diameter and grow, and altered structure and function of circulating blood cells. In some instances, the cause of a defect can be directly attributed to reduced activity of a specific copper-dependent enzyme. However, three nonspecific mechanisms of damage have been implicated in cardiovascular defects of copper deficiency. They are peroxidation, the interaction of oxygen-derived free radicals with lipids and proteins (possibly DNA); glycation, the nonenzymatic glycosylation of proteins; and nitration, the interaction of nitric oxide and its metabolites with peptides and proteins. Though independently these mechanisms present great potential for damage, the possibility that they may interact presents an added reason for concern. Furthermore, the fact that at least two of these mechanisms are associated with diabetes and aging suggests that copper deficiency may exacerbate deficits associated with these two conditions.Key words: copper, heart, circulation, peroxidation, glycation, nitric oxide.

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Rentsch, Rikke Louise, Rasmus Damsgaard, Carsten Lundby, and Carsten Juel. "Effects of darbepoetin injections on erythrocyte membrane transport protein expressions in humans." Journal of Applied Physiology 101, no. 1 (July 2006): 164–68. http://dx.doi.org/10.1152/japplphysiol.01376.2005.

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The present study investigated the effects of injected darbepoetin [novel erythropoietin stimulating protein (NESP)] on the density of three erythrocyte membrane transport proteins: the lactate-H+ cotransporter (monocarboxylate transporter 1), the chloride/bicarbonate exchanger 1 (anion exchanger 1), and the water channel aquaporin 1. Thirteen subjects were injected with NESP once a week for 4 wk. Blood samples were obtained before, during, and after the injection period, and the erythrocyte transport proteins were determined by Western blotting. The NESP injections induced a transient increase in hematocrit, red cell volume, and reticulocyte fraction. The density of aquaporin 1 protein was higher (maximal increase +59%) ( P < 0.01) during the injection period compared with the preinjection value and lower ( P < 0.01) after the injection period. The density of anion exchanger 1 protein was higher (maximal increase +15%) ( P < 0.05) during the injection period compared with the preinjection value and tended ( P = 0.06) to be lower after the injection period than before the injection period. The density of the erythrocyte monocarboxylate transporter 1 protein was higher (maximal increase +43%) ( P < 0.05) during the injection period than in the preinjection period. Age separation experiments using self-creating Percoll gradients demonstrated a higher density of membrane transport proteins in young red blood cells. These data suggest that the NESP-induced increase in membrane transport proteins is caused by a higher fraction of newly formed erythrocytes (and reticulocytes), which have a higher density of membrane transport proteins. However, increased incorporation of membrane proteins during erythrocyte formation may also be involved. We suggest that NESP improves the quality of erythrocyte membrane transport through these mechanisms.

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Kwaan, Hau C. "Role of plasma proteins in whole blood viscosity: A brief clinical review." Clinical Hemorheology and Microcirculation 44, no. 3 (2010): 167–76. http://dx.doi.org/10.3233/ch-2010-1271.

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Seth, Henrik, Erik Sandblom, and Michael Axelsson. "Nutrient-induced gastrointestinal hyperemia and specific dynamic action in rainbow trout (Oncorhynchus mykiss)—importance of proteins and lipids." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 2 (February 2009): R345—R352. http://dx.doi.org/10.1152/ajpregu.90571.2008.

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Mechanical gastric distension induces a dorsal aortic pressor response in rainbow trout ( Oncorhynchus mykiss) with no change in gastrointestinal blood flow. To elucidate what role chemical stimuli from the digested food has on the postprandial cardiovascular response, a new method was developed to investigate the contribution of individual nutrient components. Three predigested experimental diets were injected directly into the proximal intestine of rainbow trout and cardiac output (CO), gut blood flow (Qcma), heart rate (HR), and stroke volume (SV) were recorded. Specific dynamic action (SDA) was estimated by measuring oxygen consumption. When a balanced diet (50% protein, 25% fat, 15% carbohydrate) was injected, Qcma and CO increased within 1 h by 45 and 27%, respectively. The response to a high-protein diet (70% protein, 5% fat, 15% carbohydrate) was quantitatively similar but delayed, with a maximal blood flow response after 2 h. With a high-lipid diet (60% fat, 15% protein, 15% carbohydrate), the peak increase in Qcma by 22% occurred after 30 min and thereafter declined rapidly. The SDA response (19%) to the balanced diet was temporally matched with the hyperemia. With a high-protein diet, the response is delayed and enlarged (34%) compared with the balanced diet. The high-lipid diet gave no significant SDA response. We conclude that the chemical composition of the food influences the postprandial hyperemia and the SDA, such that the components appear to work in a synergistic fashion. The present results also demonstrate that both redistribution of blood flow and an overall increase in CO contribute to the postprandial increase in gut blood flow in this species.

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NYGREN, H., J. H. ELAM, and M. STENBERG. "Adsorption of coagulation proteins and adhesion and activation of platelets at the blood-solid interface. An experimental study of human whole blood." Acta Physiologica Scandinavica 133, no. 4 (August 1988): 573–77. http://dx.doi.org/10.1111/j.1748-1716.1988.tb08443.x.

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Anderson, G. Harvey. "Proteins and amino acids: effects on the sympathetic nervous system and blood pressure regulation." Canadian Journal of Physiology and Pharmacology 64, no. 6 (June 1, 1986): 863–70. http://dx.doi.org/10.1139/y86-149.

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Many functions of the brain and the sympathetic adrenal system are influenced by those amino acids that exert precursor control over neurotransmitter synthesis. One of the functions affected is regulation of blood pressure. Therefore, the purpose of this review is to describe how food proteins and amino acids affect the synthesis of neurotransmitters and their regulation of blood pressure.

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Ehrhart, I. C., L. L. McCloud, S. E. Orfanos, J. D. Catravas, and W. F. Hofman. "Effect of high blood flow on pulmonary vascular permeability to protein." Journal of Applied Physiology 76, no. 6 (June 1, 1994): 2342–47. http://dx.doi.org/10.1152/jappl.1994.76.6.2342.

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The elevated cardiac output associated with exercise increases lung lymph flow and may increase extravascular lung water. However, it is not known if extremely elevated cardiac output alters pulmonary vascular permeability. The hematocrit-protein method was used to determine the solvent drag reflection coefficient, an index of vascular permeability to proteins, in the isolated blood-perfused canine lung lobe. Microvascular pressure was obtained by double vascular occlusion. Lobes filtered fluid during perfusion at normal flow, 0.451 +/- 0.005 l/min (LF; n = 8), or high flow, 2.319 +/- 0.080 l/min (HF; n = 7). In the LF, venous pressure was elevated to 19.0 +/- 0.5 Torr to induce filtration, whereas Pv was 3.3 +/- 0.1 Torr in the HF. In HF vs. LF, respectively, arterial pressure was 61.4 +/- 7.1 vs. 28.0 +/- 1.0 Torr (P < 0.05), microvascular pressure was 31.9 +/- 3.0 vs. 22.2 +/- 0.9 Torr (P < 0.05), and sigma was 0.52 +/- 0.07 vs. 0.51 +/- 0.02 (P > 0.05). The fivefold increase in blood flow did not alter pulmonary vascular permeability to proteins; however, the capillary filtration coefficient was fivefold greater in the HF vs. LF group (0.328 +/- 0.059 vs. 0.067 +/- 0.007; P < 0.002). These data are compatible with enzyme activity measures indicating a direct linear relationship between blood flow rate and perfused pulmonary microvascular surface area. Although the data do not rule out the possibility of increased pulmonary vascular permeability to water during very elevated blood flow rates, the greater filtration rate during elevated flow is more likely related to increases in both microvascular pressure and surface area.

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Valério, Patricia, Simeon Agathopoulos, A. J. Calado, M. Fatima Leite, and Alfredo Goes. "Attachment of Blood Cells onto ZrO₂ and SiO₂-Containing Glass." Key Engineering Materials 284-286 (April 2005): 671–74. http://dx.doi.org/10.4028/www.scientific.net/kem.284-286.671.

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Samples of zirconia and a bioinert SiO2-containing glass with different surface roughness were immersed into human whole blood for different settling times to investigate the adhesion and attachment of blood cells onto these materials. The cell/material interface was directly observed by scanning electron microscopy (SEM). The results indicate that the blood cells preserved their physiology and attaching capability regardless the type of material, surface roughness, and settling time. The SEM images strongly indicate the normal function of adhesion proteins.

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Clarkson, Priscilla M., Eric P. Hoffman, Edward Zambraski, Heather Gordish-Dressman, Amy Kearns, Monica Hubal, Brennan Harmon, and Joseph M. Devaney. "ACTN3 and MLCK genotype associations with exertional muscle damage." Journal of Applied Physiology 99, no. 2 (August 2005): 564–69. http://dx.doi.org/10.1152/japplphysiol.00130.2005.

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Strenuous exercise results in damage to skeletal muscle that is manifested in delayed muscle pain, prolonged strength loss, and increases in muscle proteins in the blood, especially creatine kinase (CK) and myoglobin (Mb). Some individuals experience profound changes in these variables in response to standard laboratory exercise or recreational activities. We proposed that variations in genes coding for two myofibrillar proteins [α-actinin 3 (ACTN3) and myosin light chain kinase (MLCK)] may explain the large variability in the response to muscle-damaging exercise. We hypothesized that subjects with specific single nucleotide polymorphisms (SNPs) in ACTN3 and MLCK would show a greater loss in muscle strength and/or a greater increase in blood CK and Mb in response to eccentric exercise. Blood from 157 subjects who performed a standard elbow flexion eccentric exercise protocol was tested for association between genotypes of ACTN3 (1 SNP tested: R577X) and MLCK (2 SNPs tested: C49T and C37885A) and changes in blood CK and Mb and isometric strength. Subjects possessing the ACTN3-deficient genotype (XX) had lower baseline CK compared with the heterozygotes ( P = 0.035). After the eccentric exercise, those subjects homozygous for the MLCK 49T rare allele had a significantly greater increase in CK and Mb ( P < 0.01) compared with the heterozygotes, and those heterozygous for MLCK C37885A had a significantly greater increase in CK compared with the homozygous wild type ( P < 0.05). There was only one subject homozygous for the rare MLCK 37885A allele. MLCK C37885A was also associated with postexercise strength loss ( P < 0.05); the heterozygotes demonstrated greater strength loss compared with the homozygous wild type (CC). These results show that variations in genes coding for specific myofibrillar proteins influence phenotypic responses to muscle damaging exercise.

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Larina, I. M., A. G. Brzhzovsky, A. M. Nosovsky, M. I. Indeykina, A. S. Kononikhin, E. N. Nikolaev, and O. I. Orlov. "Oxidative Posttranslational Modifications of Blood Plasma Proteins of Cosmonauts after a Long-Term Flight: Part II." Human Physiology 47, no. 4 (July 2021): 438–47. http://dx.doi.org/10.1134/s0362119721040095.

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Reiber, Hansotto. "Cerebrospinal fluid - physiology, analysis and interpretation of protein patterns for diagnosis of neurological diseases." Multiple Sclerosis Journal 4, no. 3 (June 1998): 99–107. http://dx.doi.org/10.1177/135245859800400302.

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The state of the art in routine CSF analysis is reviewed with particular reference to multiple sclerosis regarding: (1) The physiology and pathophysiology of blood-CSF barrier function and dysfunction with the CSF flow rate as main modulator of blood- and brain-derived protein concentrations in CSF; (2) The neuroimmunological aspects regarding (a) patterns of disease-related immunoglobulin class response (IgG, lgA, IgM) in actual Reiber graphs with reference to specific parameters and optional tests, and (b) the oligoclonal, polyspecific antibody synthesis in brain; (3) Particular marker proteins in CSF and blood for differential diagnosis of neurological diseases; (4) Mathematical base for evaluations of CSF data with an example of a multiple sclerosis patient for calculation of intrathecal immunoglobulin and antibody synthesis as well as Antibody Index.

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Sarkar, Oli, Yuan Li, and Madhu B. Anand-Srivastava. "Resveratrol prevents the development of high blood pressure in spontaneously hypertensive rats through the inhibition of enhanced expression of Giα proteins." Canadian Journal of Physiology and Pharmacology 97, no. 9 (September 2019): 872–79. http://dx.doi.org/10.1139/cjpp-2019-0040.

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Resveratrol (RV), a polyphenolic component of red wine, has been shown to attenuate high blood pressure (BP) in spontaneously hypertensive rats (SHRs). We previously found that the enhanced expression of Giα proteins plays a role in the pathogenesis of hypertension in SHRs. In the present study, we investigated whether this RV-induced decrease in BP in SHRs can be attributed to the ability of RV to inhibit the enhanced expression of Giα proteins and the upstream signaling molecules implicated in the overexpression of Giα proteins. Administration of RV (50 mg/kg per day) to prehypertensive 2-week-old SHRs for 6 weeks prevented the development of high BP and inhibited the enhanced expression of Giα proteins, the enhanced levels of superoxide anion (O2−) and NADPH oxidase activity, the enhanced activation (phosphorylation) of c-Src and growth factor receptors, as well as the enhanced levels of extracellular signal-regulated kinase 1/2 (ERK1/2) and protein kinase B (Akt) exhibited by vascular smooth muscle cells isolated from SHRs. In conclusion, these results indicate that RV attenuates the development of high BP in SHRs through the inhibition of enhanced levels of Giα proteins, oxidative stress, and the upstream signaling molecules that contribute to the overexpression of Giα proteins. These findings suggest that RV could potentially be used as a therapeutic agent in the treatment of cardiovascular complications including hypertension.

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Wolf, Matthew B., and Edward C. DeLand. "A mathematical model of blood-interstitial acid-base balance: application to dilution acidosis and acid-base status." Journal of Applied Physiology 110, no. 4 (April 2011): 988–1002. http://dx.doi.org/10.1152/japplphysiol.00514.2010.

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We developed mathematical models that predict equilibrium distribution of water and electrolytes (proteins and simple ions), metabolites, and other species between plasma and erythrocyte fluids (blood) and interstitial fluid. The models use physicochemical principles of electroneutrality in a fluid compartment and osmotic equilibrium between compartments and transmembrane Donnan relationships for mobile species. Across the erythrocyte membrane, the significant mobile species Cl−is assumed to reach electrochemical equilibrium, whereas Na+and K+distributions are away from equilibrium because of the Na+/K+pump, but movement from this steady state is restricted because of their effective short-term impermeability. Across the capillary membrane separating plasma and interstitial fluid, Na+, K+, Ca2+, Mg2+, Cl−, and H+are mobile and establish Donnan equilibrium distribution ratios. In each compartment, attainment of equilibrium by carbonates, phosphates, proteins, and metabolites is determined by their reactions with H+. These relationships produce the recognized exchange of Cl−and bicarbonate across the erythrocyte membrane. The blood submodel was validated by its close predictions of in vitro experimental data, blood pH, pH-dependent ratio of H+, Cl−, and HCO3−concentrations in erythrocytes to that in plasma, and blood hematocrit. The blood-interstitial model was validated against available in vivo laboratory data from humans with respiratory acid-base disorders. Model predictions were used to gain understanding of the important acid-base disorder caused by addition of saline solutions. Blood model results were used as a basis for estimating errors in base excess predictions in blood by the traditional approach of Siggaard-Andersen (acid-base status) and more recent approaches by others using measured blood pH and Pco2values. Blood-interstitial model predictions were also used as a basis for assessing prediction errors of extracellular acid-base status values, such as by the standard base excess approach. Hence, these new models can give considerable insight into the physicochemical mechanisms producing acid-base disorders and aid in their diagnoses.

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Maron, M. B., and C. F. Pilati. "Effect of papaverine on pulmonary vascular permeability to proteins." Journal of Applied Physiology 65, no. 3 (September 1, 1988): 1367–71. http://dx.doi.org/10.1152/jappl.1988.65.3.1367.

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Previous studies have suggested that papaverine, a drug commonly used in studies of transvascular fluid and solute exchange to eliminate confounding effects of changes in vascular tone, may itself increase vascular permeability. In this study, we determined the ability of papaverine to alter pulmonary vascular protein permeability by measuring the osmotic reflection coefficient (sigma) for total proteins in a canine isolated perfused left lower lung lobe (LLL) preparation. The reflection coefficient, determined by the hematocrit-protein double-indicator technique, for control LLL's was 0.83 +/- 0.04 (SE) (n = 7). In separate groups of LLL's, blood papaverine HCl concentrations of 10(-5), 10(-4), and 10(-3) M resulted in sigma's of 0.84 +/- 0.02 (n = 6), 0.73 +/- 0.04 (n = 7), and 0.53 +/- 0.04 (n = 6), respectively. When two LLL's from the 10(-4) M group with sigma's of 0.56 and 0.57 were excluded from the analysis, the average sigma for this group was 0.79 +/- 0.02. We conclude that papaverine increases protein permeability at a concentration of 10(-3) M but does so in only some lobes at 10(-4) M. These results suggest that caution be taken when using high concentrations of papaverine in fluid balance studies.

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Muravlyova, L. E., V. B. Molotov-Luchanskiy, D. A. Kluev, and E. A. Kolesnikova. "Oxidized proteins in blood of patients with very severe chronic obstructive pulmonary disease." Free Radical Biology and Medicine 65 (September 2013): S39—S40. http://dx.doi.org/10.1016/j.freeradbiomed.2013.08.055.

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Brooks, Tracy A., Brian T. Hawkins, Jason D. Huber, Richard D. Egleton, and Thomas P. Davis. "Chronic inflammatory pain leads to increased blood-brain barrier permeability and tight junction protein alterations." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 2 (August 2005): H738—H743. http://dx.doi.org/10.1152/ajpheart.01288.2004.

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The blood-brain barrier (BBB) maintains brain homeostasis by limiting entry of substances to the central nervous system through interaction of transmembrane and intracellular proteins that make up endothelial cell tight junctions (TJs). Recently it was shown that the BBB can be modulated by disease pathologies including inflammatory pain. This study examined the effects of chronic inflammatory pain on the functional and molecular integrity of the BBB. Inflammatory pain was induced by injection of complete Freund's adjuvant (CFA) into the right plantar hindpaw in female Sprague-Dawley rats under halothane anesthesia; control animals were injected with saline. Edema and hyperalgesia were assessed by plethysmography and infrared paw-withdrawal latency. At 72 h postinjection, significant edema formation and hyperalgesia were noted in the CFA-treated rats. Examination of permeability of the BBB by in situ perfusion of [14C]sucrose while rats were under pentobarbital anesthesia demonstrated that CFA treatment significantly increased brain sucrose uptake. Western blot analysis of BBB TJ proteins showed no change in expression of zonula occludens-1 (an accessory protein) or actin (a cytoskeletal protein) with CFA treatment. Expression of the transmembrane TJ proteins occludin and claudin-3 and -5 significantly changed with CFA treatment with a 60% decrease in occludin, a 450% increase in claudin-3, and a 615% increase in claudin-5 expression. This study demonstrates that during chronic inflammatory pain, alterations in BBB function are associated with changes in specific transmembrane TJ proteins.

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Bentley, PJ. "The Crystalline Lens of the Eye: An Organismal Microcosm." Physiology 1, no. 6 (December 1, 1986): 195–99. http://dx.doi.org/10.1152/physiologyonline.1986.1.6.195.

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The lens of the eye is transparent due to several special characteristics, including the lack of a blood supply, a tight geometric arrangement of its cells, and high concentrations of special proteins called crystallins, which in solution provide a transparent medium. Opacities of the lens (cataracts), which are especially prevalent in old age, appear to result from damage to lens proteins and cell membranes. Causes of such damage include radiation, sunlight toxic chemicals and drugs, and, of special current interest, naturally occurring oxidants.

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43

Liu, Jun-hua, Ting-ting Xu, Yu-jie Liu, Wei-yun Zhu, and Sheng-yong Mao. "A high-grain diet causes massive disruption of ruminal epithelial tight junctions in goats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 305, no. 3 (August 1, 2013): R232—R241. http://dx.doi.org/10.1152/ajpregu.00068.2013.

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Alterations in rumen epithelial tight junctions (TJs) at the tissue and molecular levels during high-grain (HG) diet feeding are unknown. Here, 10 male goats were randomly assigned to either a hay diet (0% grain; n = 5) or HG diet group (65% grain; n = 5) to characterize the changes in ruminal epithelial structure and TJ protein expression and localization using scanning and transmission electron microscopy, quantitative real-time PCR, Western blot analysis, and immunofluorescence. After 7 wk of feeding, ruminal free LPS in HG group increased significantly ( P < 0.001) compared with the hay group, and free LPS in the peripheral blood was detectable with concentrations of 0.8 ± 0.20 EU/ml, while not detectable in the control, suggesting a leakage of LPS into the blood in the HG group. Correspondingly, the HG-fed goats showed profound alterations in ruminal epithelial structure and TJ proteins, depicted by marked epithelial cellular damage and intercellular junction erosion, down-regulation of TJ proteins claudin-4, occludin, and zonula occludens-1 mRNA and protein expression, as well as redistribution of claudin-1, claudin-4, and occludin. Furthermore, these changes in TJ proteins in the HG group were coupled with the upregulation of mRNA levels for the cytokines TNF-α and IFN-γ in the ruminal epithelia. These results demonstrated for the first time that the HG diet feeding caused disruption of ruminal epithelial TJs that was associated with a local inflammatory response in the rumen epithelium. These findings may provide new insights into understanding the role of TJ proteins in the ruminal epithelial immune homeostasis of ruminants.

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Lu, Yan, David E. Stec, Ruisheng Liu, Michael Ryan, and Heather A. Drummond. "βENaC and ASIC2 associate in VSMCs to mediate pressure-induced constriction in the renal afferent arteriole." American Journal of Physiology-Renal Physiology 322, no. 5 (May 1, 2022): F498—F511. http://dx.doi.org/10.1152/ajprenal.00003.2022.

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Transmission of systemic blood pressure to delicate renal microvessels is a primary determinant of vascular injury in chronic kidney disease progression to end-stage renal disease. Here, we identified two degenerin family members, with an evolutionary link to mechanosensing, that interact biochemically and functionally to regulate systemic blood pressure and renal injury. Thus, degenerin proteins may serve as a target for the development of therapies to prevent or delay renal disease progression.

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Gliński, Z., J. Jarosz, and A. Wernicki. "Serological characterization of soluble proteins in greater wax moth larval blood." Comparative Biochemistry and Physiology Part B: Comparative Biochemistry 84, no. 1 (January 1986): 131–35. http://dx.doi.org/10.1016/0305-0491(86)90282-8.

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Yang, Y., M. Zhou, and H. Liu. "Luteolin, an aryl hydrocarbon receptor antagonist, alleviates diabetic retinopathy by regulating the NLRP/NOX4 signalling pathway: Experimental and molecular docking study." Physiology International 108, no. 2 (July 9, 2021): 172–84. http://dx.doi.org/10.1556/2060.2021.00148.

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AbstractObjectiveThe present report evaluates the protective effects of luteolin against diabetic retinopathy (DR).Materials and methodsDiabetes was induced in rats by i.p. administration of 60 mg/kg of streptozotocin (STZ), followed by treatment with luteolin for 4 weeks. The effects of luteolin were determined based on the blood glucose and cytokine levels, and parameters of oxidative stress in retinal tissue of DR rats. The diameter of retinal vessels was estimated by fundus photography. A Western blot assay was used to determine the expression of apoptotic proteins and Nod-like receptor 3 (NLRP3) pathway proteins in the retina of DR rats. A molecular docking study was performed to evaluate the interaction between luteolin and NLRP3.ResultsThe level of blood glucose was reduced in the luteolin-treated group compared with the DR group. Reductions in cytokines and oxidative stress were observed in the retinal tissues of the luteolin-treated group relative to the DR group. Moreover, treatment with luteolin reduced the expression of NLRP1, NOX4, TXNIP, and NLRP3 proteins, and ameliorated the altered expression of apoptotic proteins in the retina of DR rats.ConclusionIn conclusion, luteolin prevents retinal apoptosis in DR rats by regulating the NLRP/NOX4 signalling pathway.

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Larina, I. M., A. G. Brzhzovsky, A. M. Nosovsky, A. S. Kononikhin, and O. I. Orlov. "Post-Translational Oxidation Modifications of Blood Plasma Proteins of Cosmonauts after a Long-term Flight: Part I." Human Physiology 46, no. 5 (September 2020): 531–39. http://dx.doi.org/10.1134/s0362119720050072.

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Sayer, J. A., and S. H. S. Pearce. "Diagnosis and Clinical Biochemistry of Inherited Tubulopathies." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 38, no. 5 (September 2001): 459–70. http://dx.doi.org/10.1177/000456320103800503.

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Epithelial ion channels and transporter proteins have physiologically important roles throughout the length of the nephron. Discovering the molecular identities of tubular epithelial cell proteins and their functional roles has increased understanding of both renal physiology and tubular diseases. Defects in tubular handling of solutes may present with nephrocalcinosis or nephrolithiasis, rickets, acid-base, electrolyte or blood pressure disturbances. Biochemical analysis of both serum and urine, together with clinical history and examination, remain fundamental for their diagnosis, whilst understanding of underlying molecular mechanisms allows appropriate management.

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Lux, Samuel E. "Anatomy of the red cell membrane skeleton: unanswered questions." Blood 127, no. 2 (January 14, 2016): 187–99. http://dx.doi.org/10.1182/blood-2014-12-512772.

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Abstract The red cell membrane skeleton is a pseudohexagonal meshwork of spectrin, actin, protein 4.1R, ankyrin, and actin-associated proteins that laminates the inner membrane surface and attaches to the overlying lipid bilayer via band 3–containing multiprotein complexes at the ankyrin- and actin-binding ends of spectrin. The membrane skeleton strengthens the lipid bilayer and endows the membrane with the durability and flexibility to survive in the circulation. In the 36 years since the first primitive model of the red cell skeleton was proposed, many additional proteins have been discovered, and their structures and interactions have been defined. However, almost nothing is known of the skeleton’s physiology, and myriad questions about its structure remain, including questions concerning the structure of spectrin in situ, the way spectrin and other proteins bind to actin, how the membrane is assembled, the dynamics of the skeleton when the membrane is deformed or perturbed by parasites, the role lipids play, and variations in membrane structure in unique regions like lipid rafts. This knowledge is important because the red cell membrane skeleton is the model for spectrin-based membrane skeletons in all cells, and because defects in the red cell membrane skeleton underlie multiple hemolytic anemias.

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Cho, Sung Hoon, Shreevrat Goenka, Tiina Henttinen, Prathyusha Gudapati, Arja Reinikainen, Christine M. Eischen, Riitta Lahesmaa, and Mark Boothby. "PARP-14, a member of the B aggressive lymphoma family, transduces survival signals in primary B cells." Blood 113, no. 11 (March 12, 2009): 2416–25. http://dx.doi.org/10.1182/blood-2008-03-144121.

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Poly(ADP-ribos)ylation is one of the longest-known but most enigmatic posttranslational modifications transducing specific signals. The enzyme responsible for the majority of poly(ADP-ribose) polymerization in cells, PARP-1, promotes DNA repair but also mediates a caspase-independent form of apoptosis in response to stressors such as irradiation. However, the biologic function of most other PARPs is not known. Macro-PARPs constitute one branch of the large family of PARP-like proteins also designated as B aggressive lymphoma proteins (BAL1, 2a/2b, 3, or PARP-9, PARP-14, and PARP-15). To elucidate biologic role(s) of a BAL-family macro-PARP, we analyzed mice deficient in PARP-14, a binding partner of the IL-4–induced transcription factor Stat6. We show here that PARP-14 plays a fundamental role mediating protection against apoptosis in IL-4–treated B cells, including that after DNA damage, and mediates IL-4 effects on the levels of gene products that regulate cell survival, proliferation, and lymphomagenesis. Collectively, the results establish that PARP-14 mediates regulation of gene expression and lymphocyte physiology by IL-4 and has a function distinct from PARP-1. Furthermore, the findings suggest mechanisms by which BAL-family proteins might influence pathologic processes involving B lymphocytes.

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Journal articles on the topic 'Blood proteins Physiology'

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