Academic literature on the topic 'ENOS protein expression'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'ENOS protein expression.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "ENOS protein expression"
1
ARRIERO, MARÍA M., JUAN A. RODRÍGUEZ-FEO, ÁNGEL CELDRÁN, LOURDES SÁNCHEZ DE MIGUEL, FERNANDO GONZÁLEZ-FERNÁNDEZ, JOSÉ FORTES, ANA REYERO, et al. "Expression of Endothelial Nitric Oxide Synthase in Human Peritoneal Tissue." Journal of the American Society of Nephrology 11, no. 10 (October 2000): 1848–56. http://dx.doi.org/10.1681/asn.v11101848.
Full textAbstract:
Abstract. Changes in the expression of endothelial nitric oxide synthase (eNOS) in the peritoneum could be involved in the peritoneal dysfunction associated with peritoneal inflammation. Demonstrated recently in bovine endothelial cells was the existence of cytosolic proteins that bind to the 3′-untranslated region (3′-UTR) of eNOS mRNA and could be implicated in eNOS mRNA stabilization. The present work demonstrates that eNOS protein is expressed in human endothelial and mesothelial peritoneal cells. Escherichia coli lipopolysaccharide shortened the half-life of eNOS message, reducing eNOS protein expression in peritoneal mesothelial and endothelial cells. Moreover, under basal conditions, human peritoneal samples expressed cytosolic proteins that bind to the 3′-UTR of eNOS mRNA. The cytosolic proteins that directly bind to 3′-UTR were identified as a 60-kD protein. After incubation of human peritoneal samples with lipopolysaccharide, the binding activity of the cytosolic 60-kD protein increased in a time-dependent manner. Studies are now necessary to determine the involvement of this 60-kD protein in the regulation of eNOS expression in peritoneal cells and particularly its involvement in the peritoneal dysfunction associated with inflammatory reactions.
2
Grazul-Bilska, Anna T., Chainarong Navanukraw, Mary Lynn Johnson, Daniel A. Arnold, Lawrence P. Reynolds, and Dale A. Redmer. "Expression of endothelial nitric oxide synthase in the ovine ovary throughout the estrous cycle." Reproduction 132, no. 4 (October 2006): 579–87. http://dx.doi.org/10.1530/rep-06-0009.
Full textAbstract:
This study was conducted to evaluate the expression of endothelial nitric oxide synthase (eNOS) in ovarian follicles and corpora lutea (CL) throughout the estrous cycle in sheep. Three experiments were conducted to (1) immunolocalize eNOS protein, (2) determine expression of mRNA for eNOS and its receptor guanylate cyclase 1 soluble β3 (GUCY1B3), and (3) co-localize eNOS and vascular endothelial growth factor (VEGF) proteins in the follicles and/or CL throughout the estrous cycle. In experiment 1, ovaries were collected from ewes treated with FSH, to induce follicular growth or atresia. In experiment 2, ovaries were collected from ewes treated with FSH and hCG to induce follicular growth and ovulation. In experiment 3, ovaries were collected from superovulated ewes to generate multiple CL on days 2, 4, 10, and 15 of the estrous cycle. In experiments 1 and 2, the expression of eNOS protein was detected in the blood vessels of the theca externa and interna of healthy ovarian follicles. However, in early and advanced atretic follicles, eNOS protein expression was absent or reduced. During the immediate postovulatory period, eNOS protein expression was detected in thecal-derived cells that appeared to be invading the granulosa layer. Expression of eNOS mRNA tended to increase in granulosa cells at 12 and 24 h, and in theca cells 48 h after hCG injection. In experiment 3, eNOS protein was located in the blood vessels of the CL during the estrous cycle. Dual localization of eNOS and VEGF proteins in the CL demonstrated that both were found in the blood vessels.
3
Ruiz-Holst, C., B. Bölck, A. Ghanem, K. Tiemann, S. Brokat, V. Regitz-Zagrosek, W. Bloch, Robert H. G. Schwinger, and K. Brixius. "eNOS phosphorylation and translocation are altered in male but not female mice by increased activation of the Gαq protein." Canadian Journal of Physiology and Pharmacology 88, no. 2 (February 2010): 121–29. http://dx.doi.org/10.1139/y09-115.
Full textAbstract:
Little is known about sex-dependent physiological and pathophysiological differences in cardiac endothelial nitric oxide synthase (eNOS) expression and activation. Therefore, we investigated cardiac morphology and eNOS protein expression, including its translocation-dependent activation and phosphorylation, in cardiac tissue of male and female wild-type mice and transgenic heart-failure mice having a cardiac-specific, 5-fold overexpression of the Gαq protein. In addition, we measured calcineurin protein expression. Heart-to-body weight ratio was increased in Gαq mice. Female wild-type mice showed higher eNOS protein expression and activation (translocation and phosphorylation) than did wild-type males. In cardiac tissue of Gαq mice, these sex-dependent differences remained or were enhanced. Protein expression of the catalytic subunit calcineurin A, which has been shown to dephosphorylate eNOS, was higher in wild-type males than in wild-type females. These differences were increased in the Gαq mice model. We conclude that sex differences exist in cardiac eNOS protein expression and phosphorylation. Increased activation of the Gαq protein appears to alter eNOS protein expression and phosphorylation only in males.
4
Li, Dechun, Victor E. Laubach, and Roger A. Johns. "Upregulation of lung soluble guanylate cyclase during chronic hypoxia is prevented by deletion of eNOS." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 2 (August 1, 2001): L369—L376. http://dx.doi.org/10.1152/ajplung.2001.281.2.l369.
Full textAbstract:
Hypoxia upregulates endothelial (e) nitric oxide synthase (NOS), but how eNOS affects soluble guanylate cyclase (sGC) protein expression in hypoxia-induced pulmonary hypertension is unknown. Wild-type (WT), eNOS-deficient [eNOS(−/−)], and inducible NOS (iNOS)-deficient [iNOS(−/−)] mice were used to investigate the effects of lack of NO from different NOS isoforms on sGC activity and protein expression and its relationship to the muscularization of the pulmonary vasculature. After 6 days of hypoxic exposure (10% O2), the ratios of the right ventricle to left ventricle + septum weight (RV/LV+S) and right ventricle weight to body weight, the lung sGC activity, and vascular muscularization were determined, and protein analysis for eNOS, iNOS, and sGC was performed. Results demonstrated that there were significant increases of RV/LV+S in all animals treated with hypoxia. In hypoxic WT and iNOS(−/−) mice, eNOS and sGC α1- and β1-protein increased twofold; cGMP levels and the number of muscularized vessels also increased compared with hypoxic eNOS(−/−) mice. There was a twofold increase of iNOS protein in WT and eNOS(−/−) mice, and the basal iNOS protein concentration was higher in eNOS(−/−) mice than in WT mice. In contrast, the eNOS(−/−) mouse lung showed no eNOS protein expression, lower cGMP concentrations, and no change of sGC protein levels after hypoxic exposure compared with its normoxic controls ( P > 0.34). These results suggest that eNOS, but not iNOS, is a major regulator of sGC activity and protein expression in the pulmonary vasculature.
5
Kim, Hee Youn, and Dong Sup Lee. "A role for phosphodiesterase type 5 inhibitors in remodelling the urinary bladder after radiation exposure." PLOS ONE 15, no. 11 (November 9, 2020): e0242006. http://dx.doi.org/10.1371/journal.pone.0242006.
Full textAbstract:
Minimizing the toxicity of radiotherapy is challenging. We investigated the effects of a phosphodiesterase type-5 inhibitor (PDE5I) on the urinary bladder after pelvic radiotherapy. Eight rats were assigned to each group (group 1: control; group 2: radiation; group 3: radiation plus PDE5I). Radiation dose was 10 Gy/one fraction. Udenafil (20 mg/kg, daily for 4 weeks) was administered in group 3. Cystometry was performed 4 weeks after treatment, followed by real-time PCR for PDE5, vascular endothelial growth factor (VEGF), and endothelial nitric oxide synthase (eNOS) mRNA, western blotting for PDE5, cyclic GMP-dependent protein kinase (PRKG), VEGF164, Akt, eNOS and NADPH oxidase (NOX)-2 proteins, and immunohistochemistry for eNOS. The expression of both VEGF mRNA and eNOS mRNA was higher in group 3 than in group 2. VEGF and eNOS protein expression improved with PDE5I treatment. Akt protein phosphorylation was higher in group 3 than in group 2, but NOX-2 protein expression was lower in group 3 than in group 2. Immunohistochemistry showed that the mean density of arterioles expressing eNOS was higher in group 3 than in group 2. Cystometry revealed that the intercontraction interval was remarkably longer in group 3 than in group 2 but that the maximal voiding pressure was higher in group 2 than in group 3. Daily treatment with a PDE5I after radiotherapy may prevent bladder storage dysfunction, potentially due to its effects on vasodilation and angiogenesis and through minimizing tissue oxidative damage by means of the VEGF/Akt/eNOS pathway.
6
North, A. J., K. S. Lau, T. S. Brannon, L. C. Wu, L. B. Wells, Z. German, and P. W. Shaul. "Oxygen upregulates nitric oxide synthase gene expression in ovine fetal pulmonary artery endothelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 4 (April 1, 1996): L643—L649. http://dx.doi.org/10.1152/ajplung.1996.270.4.l643.
Full textAbstract:
Nitric oxide (NO) is critically involved in oxygen-mediated pulmonary vasodilatation in the fetus and newborn. We determined the effects of prolonged alterations in oxygenation on endothelial NO synthase (eNOS) gene expression in early passage ovine fetal intrapulmonary artery endothelial cells (PAEC). PAEC were exposed to PO2 = 50 or 150 mmHg for 48 h, and eNOS protein expression was evaluated by immunoblot analysis. eNOS protein expression was 2.7-fold greater at higher oxygen tension; eNOS upregulation was also evident after 24 h. Inducible NOS protein was not detectable by immunoblot at either level of oxygenation. In the lung, the effect of oxygen on eNOS expression may be specific to the endothelium, as eNOS expression in bronchiolar epithelial cells of Clara cell lineage was not altered by varying oxygen tension. The oxygen-related increase in eNOS protein in the fetal PAEC was associated with 2.5-fold greater NOS enzymatic activity. In parallel, there was a 2.8-fold rise in eNOS mRNA abundance. Thus eNOS gene expression in ovine fetal PAEC is upregulated by oxygen, and this is mediated at the level of gene transcription or mRNA stability. This process may play an important role in oxygen modulation of pulmonary vasomotor tone in the fetus and newborn.
7
Ríos, Nisa Buset, Francisco Rodríguez Esparragón, and José C. Rodríguez Pérez. "Telmisartan-induced eNOS gene expression is partially independent of its PPAR-gamma agonist property." Clinical & Investigative Medicine 35, no. 2 (April 1, 2012): 55. http://dx.doi.org/10.25011/cim.v35i2.16289.
Full textAbstract:
Purpose: Telmisartan, an angiotensin II receptor blocker (ARB), also acts as an activator of peroxisome proliferator-activated receptor-gamma (PPAR-gamma; PPAR-γ). Several studies have explored the PPAR-γ-endothelial nitric oxide synthase (eNOS) pathway associated with improvement of endothelial function by telmisartan. The ability of telmisartan to induce gene expression and protein level of eNOS and PPARγ in adipocytes was investigated. Methods: Expression of aP2, PPARγ, eNOS and iNOS genes were measured using the quantitative real-time polymerase chain reaction. The changes, at the protein level, were explored by Western blot, which evaluated the native and phosphorylated eNOS forms, eNOS-Ser1177 and eNOS-Thr495. Results: Adipocytes, exposed to telmisartan, exhibited an increase in PPARγ gene expression but a decrease in protein level. Nonetheless, after the exposure to telmisartan, eNOS-Ser1177 phosphorylation, associated with eNOS activity increment, reached its highest value while eNOS-Thr495 phosphorylation, involved in the inhibition of eNOS activity, showed its lowest value. Conclusion: The results suggest that telmisartan preserves eNOS activity via a mechanism that is partially independent of the PPARγ-eNOS pathway in adipocytes.
8
de Frutos, Trinidad, Lourdes Sánchez de Miguel, Margarita García-Durán, Fernando González-Fernández, Juan A. Rodríguez-Feo, Mercedes Montón, José Guerra, Jerónimo Farré, Santos Casado, and Antonio López-Farré. "NO from smooth muscle cells decreases NOS expression in endothelial cells: role of TNF-α." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 4 (October 1, 1999): H1317—H1325. http://dx.doi.org/10.1152/ajpheart.1999.277.4.h1317.
Full textAbstract:
Despite the evidence that cytokines stimulate nitric oxide (NO) production by inducible nitric oxide synthase (iNOS), several reports recently demonstrated that the hypotensive response related to endothelial nitric oxide synthase (eNOS) activity could be inhibited by the same cytokines. The aim of the present work was to analyze whether NO generated by vascular smooth muscle cells (VSMC) could modify eNOS protein expression in endothelial cells. Bovine aortic endothelial cells (BAEC) and bovine VSMC (BVSMC) in coculture were used for the study. Interleukin-1β (IL-1β, 10 ng/ml)-treated BVSMC, which expressed iNOS protein, decreased eNOS protein expression in BAEC. The presence of NO antagonists N ω-nitro-l-arginine methyl ester (10−3 mol/l) or N G-monomethyl-l-arginine (10−3 mol/l) prevented the decrease in eNOS protein expression induced by IL-1β-treated BVSMC. Surprisingly, two different NO donors, 3-morpholinosydnonimine (10−4 mol/l) and S-nitroso- N-acetyl-d,l-penicillamine (10−4 mol/l), failed to modify eNOS expression in BAEC, suggesting the existence of a diffusible mediator released from IL-1β-treated BVSMC that acts on endothelial cells by reducing eNOS expression. The presence of NO antagonists reduced tumor necrosis factor-α (TNF-α) production by IL-1β-stimulated BVSMC. This effect was also produced in the presence of a protein kinase G inhibitor, guanosine-5′-O-(2-thiodiphosphate) trilithium salt. A polyclonal antibody against TNF-α prevented eNOS expression in the BAEC-BVSMC coculture. In conclusion, NO by itself failed to modify eNOS protein expression in endothelial cells but increased TNF-α generation by IL-1β-stimulated BVSMC and, in this way, reduced eNOS expression in the endothelium.
9
Shaul, P. W., I. S. Yuhanna, Z. German, Z. Chen, R. H. Steinhorn, and F. C. Morin. "Pulmonary endothelial NO synthase gene expression is decreased in fetal lambs with pulmonary hypertension." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 5 (May 1, 1997): L1005—L1012. http://dx.doi.org/10.1152/ajplung.1997.272.5.l1005.
Full textAbstract:
Nitric oxide (NO), produced by endothelial (e) NO synthase (NOS), is critically involved in the cardiopulmonary transition from fetal to neonatal life. We have previously shown that NO-dependent relaxation is attenuated in intrapulmonary arteries from fetal lambs with pulmonary hypertension (PHT) created by prenatal ligation of the ductus arteriosus. In the present study, we determined whether this is due to altered pulmonary eNOS expression. eNOS and neuronal NOS (nNOS) protein expression were assessed in lungs from near-term control lambs and PHT lambs that underwent ductal ligation 10 days earlier. eNOS protein expression was decreased 49% in PHT lung. In contrast, nNOS protein abundance was unchanged. NOS enzymatic activity was also diminished in PHT vs. control lung (60 +/- 3 vs. 110 +/- 7 fmol.mg protein-1.min-1, respectively). Paralleling the declines in eNOS protein and NOS enzymatic activity, eNOS mRNA abundance was decreased 64% in PHT lung. Thus pulmonary eNOS gene expression is attenuated in the lamb model of fetal PHT. Because NO modulates both vasodilation and vascular smooth muscle growth, diminished eNOS expression may contribute to both the abnormal vasoreactivity and the excessive muscularization of the pulmonary circulation in fetal PHT.
10
Parker, Thomas A., Timothy D. le Cras, John P. Kinsella, and Steven H. Abman. "Developmental changes in endothelial nitric oxide synthase expression and activity in ovine fetal lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 278, no. 1 (January 1, 2000): L202—L208. http://dx.doi.org/10.1152/ajplung.2000.278.1.l202.
Full textAbstract:
Endothelial nitric oxide (NO) synthase (eNOS) produces NO, which contributes to vascular reactivity in the fetal lung. Pulmonary vasoreactivity develops during late gestation in the ovine fetal lung, during the period of rapid capillary and alveolar growth. Although eNOS expression peaks near birth in the fetal rat, lung capillary and distal air space development occur much later than in the fetal lamb. To determine whether lung eNOS expression in the lamb differs from the timing and pattern reported in the rat, we measured eNOS mRNA and protein by Northern and Western blot analyses and NOS activity by the arginine-to-citrulline conversion assay in lung tissue from fetal, newborn, and maternal sheep. Cellular localization of eNOS expression was determined by immunohistochemistry. eNOS mRNA, protein, and activity were detected in samples from all ages, and eNOS was expressed predominantly in the vascular endothelium. Lung eNOS mRNA expression increases from low levels at 70 days gestation to peak at 113 days and remains high for the rest of fetal life. Newborn eNOS mRNA expression does not change from fetal levels but is lower in the adult ewe. Lung eNOS protein expression in the fetus rises and peaks at 118 days gestation but decreases before birth. eNOS protein expression rises in the newborn period but is lower in the adult. Lung NOS activity also peaks at 118 days gestation in the fetus before falling in late gestation and remaining low in the newborn and adult. We conclude that the pattern of lung eNOS expression in the sheep differs from that in the rat and may reflect species-related differences in lung development. We speculate that the rise in fetal lung eNOS may contribute to the marked lung growth and angiogenesis that occurs during the same period of time.
Dissertations / Theses on the topic "ENOS protein expression"
1
Park, Joon Young. "NFKB1 gene promoter polymorphism and unidirectional laminar shear stress implications for NF-kB activation, eNOS protein expression and endothelial function /." College Park, Md. : University of Maryland, 2006. http://hdl.handle.net/1903/3646.
Full textAbstract:
Thesis (Ph. D.) -- University of Maryland, College Park, 2006.Thesis research directed by: Kinesiology. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
2
Yi, Xiaoqin. "Total ginsenosides of Asian ginseng increase coronary artery perfusion flow of the ischemia-reperfusion injury rat heart in Langendorff system through activation of Akt-eNOS signaling and cardiac energy-associate protein expression." HKBU Institutional Repository, 2010. http://repository.hkbu.edu.hk/etd_ra/1195.
Full text
3
Kucharova, Veronika. "Expression of recombinant proteins in Escherichia coli: The influence of the nucleotide sequences at the 5´ ends of target genes." Doctoral thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for bioteknologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-17668.
Full textAbstract:
The nucleotide sequence at the 5´ end of genes can be specified as the sequence of a promoter associated 5´ untranslated region (UTR) together with the initial coding sequence of a gene. Because this genetic region has been implicated in the control of translation, messenger RNA (mRNA) stability and even transcription, it can be looked at as one of the central control points in gene expression. Both the 5´-UTR and the coding sequence have often been included in optimization strategies targeted to simulate recombinant protein production in E. coli and numerous reports describe various sequence-dependent structural features that can positively influence the overall expression process. Nevertheless, the actual mechanisms by which the regulation of gene expression is exerted at the 5´ end remain obscure. The work reported in this thesis has involved various types of analyses of the functionality of the 5´ end, by using mutations as a major tool. The work can be seen as mainly a detailed empirical analysis of the relation between the specific nucleotide sequences at the 5’ end of genes and the final outcome at the protein production level. The results also indicate that optimizations based on empirical laboratory protocols are currently unlikely to be exceeded by predictions based on bioinformatics software. Sequence mutagenesis of elements in the XylS/Pm - positive regulator/promoter system coupled to high-throughput screening had been previously proven to be a powerful method for increasing the expression of recombinant genes from this expression cassette. At the beginning of this thesis work the effect of introducing random mutations in the DNA sequence of the Pm promoter associated 5´-UTR and two 5´ fusion partners, whose sequences correspond either to a consensus translocation signal peptide or the first 23 codons of a well-expressed celB gene (encoding a cytoplasmic phosphoglucomutase) was investigated. The core of the experimental work was construction of large combinatorial libraries of the different DNA sequences and subsequent selection for improved expression of a reporter gene (either ampicillin or apramycin resistance gene), that was indicated by an increase in antibiotic tolerance of the corresponding E. coli host cells. A shared result of the three individual studies was the establishment of a collection of optimized sequences that generally improved protein production properties of both reporter and industrially relevant heterologous genes. In addition to random mutagenesis, also synonymous mutations were introduced in the DNA sequence of the consensus signal peptide (CSP) and the consequent expression effects were evaluated. As a conclusion, the DNA changes that did not alter the amino acid sequence led to a lesser stimulation of expression of the bla reporter (ampicillin resistance) than when complete sequence randomization was applied. Moreover, similar results were obtained when synonymous codon usage of the first 9 codons of the medically important ifn-α2b gene was optimized by a bioinformatic method, followed by experimental determination of expression levels of several rationally selected ifn-α2b synonymous variants. These results indicated that optimization of the codon usage of the 5´ coding sequence has limited effects, probably due to the sequence intrinsic characteristics. However, the use of optimized 5´ fusion partners or 5´-UTR variants can often overcome such limitations. Besides evaluating the expression at the protein level, the work also addressed how the changes of the 5´ end of a gene influence expression at the level of transcript accumulation and mRNA stability. For that purpose, a non-invasive method for accessing recombinant mRNA stability in bacteria was developed. The procedure was based on the removal of diffusible transcriptional inducers followed by qRT-PCR determination of mRNA levels at consecutive time-points. Among the principal findings was that a 5´ fusion partner (specifically: translocation signals pelB and ompA, together with the celB-based 5´ fusion) contributes to the stimulation of recombinant gene expression by enhancing the stability of the corresponding fusion mRNA. The stimulation of expression caused by specific mutations in the 5´-UTR and adjacent coding sequence (synonymous changes), on the other hand, surprisingly appeared to result from improved rate of mRNA synthesis. Three selected promoter systems (Pm, Ptac and the T7 based) were used in these studies, and part of the work also evaluated how fast each system responds to addition and removal of its inducer, respectively. The expression systems were found to affect both transcript accumulation and decay in a specific way that correlated with the type of transcription regulation each system is subjected to. Finally, a study comparing five bacterial expression systems (XylS/Pm, XylS/Pm ML1-17 (a Pm variant), the bacteriophage T7 RNA polymerase/promoter system, LacI/Ptrc and AraC/PBAD) with respect to their production capacity of five different recombinant proteins was carried out. The comparison revealed many expression system and model gene specific features and that none of the systems was superior in all evaluated aspects; which included system´s adaptability, maximum protein yield, basal expression in the absence of inducer, use of cellular resources and homogeneity of expression. However, particularly because of a large associated collection of optimized genetic elements (such as sequence variants of the Pm promoter, the XylS regulator, 5´-UTR and various translocation signals) and the possibility of simple genetic adjustments that can lead to both higher and lower expression levels, the XylS/Pm system appeared as a good starting point for optimization of various kinds of protein production processes.A Combinatorial Mutagenesis Approach to Improve Microbial Expression Systems
4
Chang, Chih-Chiang, and 張志強. "Studies on the role of α-enolase(ENO1) in Breast Cancer andits Molecular Mechanism of Tamoxifen Induces α-enolase Protein Expression." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/08545714037639027551.
Full textAbstract:
碩士臺北醫學大學
醫學科學研究所
96
Enolase α(ENO1) is a cytoplasmic glycolytic enzyme involved in the formation of phosphoenolpyruvate. More recent evidence, however ,shows that Enolase is a multifunction protein.In mammalian cells,three isoforms of enolase have been found. There are designated as enolase-α(ENO1)、enolase-β(ENO3)、enolase-γ(ENO2).ENO1 is widely distributed in a variety of tissues, whereas ENO2 and ENO3 are exclusively found in neuron/neuronendocrine and muscles tissues, respectively. The expression of the those isoforms is developmentally regulated in a tissue-specific manner.Enolases from heterodimers or homodimers to convert 2-phosphoglycerate into phosphoenolpyruvate in glycolysis. Enolase αand c-myc binding protein originate from a single gene through alternative use of translational starting site. We previously demonstrated that Tamoxifen induces ENO1 expression in MCF-7 cell line. In this report, we found Tamoxifen induces ENO1、ERα、ERα p118、NFκB protein expression. In the database (TFSEARCH: Searching Transcription Factor Binding Sites),we found NFκB binding site in ENO1 promoter. Nuclear extraction suggested that Tamoxifen inducing NFκB translocation into nuclear. We use PDTC, a NFκB inhibitor, blocks NFκB tronslocation into nucleus. PDTC inhibitor was down-regulated ENO1 protein expression. We investigated NFκB regulation ENO1 expression by binding on ENO1 promoter.Quantitative assays of the mRNA levels of the ENO1 was measured by Real-time PCR analysis technique and revealed that expression of the ENO1 was higher in tumor tissue when compared to normal tissue which dissected form the tumor margin. Tissue section from patients with breast caner were examined Immunohistochemically. We found ENO1 overexpression in breast ductal carcinoma.
Book chapters on the topic "ENOS protein expression"
1
Uddandrao, V. V. Sathibabu, P. P. Sethumathi, Parim Brahma Naidu, S. Vadivukkarasi, Mustapha Sabana Begum, and G. Saravanan. "Ameliorative Potential of Biochanin-A against Dexamethasone Induced Hypertension through Modulation of Relative mRNA and Protein Expressions in Experimental Rats." In Advancements in Cardiovascular Research and Therapeutics: Molecular and Nutraceutical Perspectives, 156–70. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815050837122010011.
Full textAbstract:
In this study, we made an attempt to attenuate the dexamethasone induced hypertension through Biochanin-A (BCA) in experimental rats. Hypertension was induced in male albino Wistar rats by subcutaneous administration of dexamethasone (10μg/kg body weight). The rats were orally treated with BCA (10mg/kg body weight) once daily for 45 days and Nicorandil-treated group (6mg/kg body weight) included for comparison. We evaluated the changes in mean arterial pressure, heart rate, blood pressure, vascular function, oxidative stress markers, and gene expression of histone deacetylases (HDAC)-1, HDAC-2, and HDAC-8. Administration of BCA or Nicorandil showed noteworthy improvement in vascular function in experimental rats. Moreover, aortic eNOS expression was down regulated, and NADPH oxidase subunit p47phox was up regulated in hypertensive rats. The antihypertensive effects of BCA were connected with concomitant downregulation of p47phox expression and upregulation of eNOS expression. Dexamethasone exposure led to increased mRNA expression of HDACs expression in the kidneys and these were restored after BCA administration. In conclusion, our results are, therefore, BCA reduces hypertension in experimental rats and suggests that BCA might be used against the hypertension.
2
Williams, Jennie, Jenny Paredes, and Shrey Thaker. "Genetics of Colorectal Cancer Racial Disparities." In Gene Expression [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.103730.
Full textAbstract:
This chapter describes genetics and epigenetics discoveries that have allowed investigators to better define cancer at the molecular level. Taking into consideration the expanse of the field of cancer, the focus will be on colon cancer as a platform to provide examples of techniques, recent discoveries, and translation of genetic studies to cancer care. In addition, this segment contributes to our understanding of racial and ethnic disparities in colon cancer and the use of -omic assessments as an application in cancer research. Thus, this section will provide an overarching view of cancer by defining the molecular characteristics of colon cancer; parameters of cancer disparities; and genetic factors that contribute to colon-tumor biology, specifically recent findings at the DNA, RNA, and protein levels. Importantly, the correlation of these factors with the immune system will be defined. This section ends with future directions for studying colon cancer in patients from medically underserved communities. In summary, this unit provides an introduction to how genetic and genomic investigations are helping to elucidate biological questions in an inclusive manner that will benefit patients on a global scale.
3
Grasse, Jonathon. "Regionalist Themes in the Songs of the Corner Club." In Hearing Brazil, 239–72. University Press of Mississippi, 2022. http://dx.doi.org/10.14325/mississippi/9781496838278.003.0009.
Full textAbstract:
Chapter nine analyzes songs of the Corner Club popular music collective for regionalist themes and images. Of the primary themes found are those of bucolic rurality and the power of the natural world, the contrasting gleam of modern Belo Horizonte, poetic expressions of isolation and independence associated with Minas Gerais, and political protest punctuated with regional ideals. The chapter discusses social and political movements, the military dictatorship, revisits the viola (particularly in the work of Tavinho Moura), and ends with a return to themes of local Afro-Mineiro music culture as discovered in the early 2000s work of Corner Club leader Milton Nascimento. The chapter presents brief biographical sketches of collective members, their deep family connections to Minas Gerais, and some of their roles in the collective's discography. Through key collective members Lô Borges and Beto Guedes, rock is seen as a new strata of 1960s-70s identity in Belo Horizonte.
Conference papers on the topic "ENOS protein expression"
1
Ye, Jianfeng, Baoguo Chen, and Lisa X. Xu. "Shear Stress Effect on the Production of Nitric Oxide in Cultured Rat Aorta Endothelial Cells." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-33074.
Full textAbstract:
Atherosclerotic lesions tend to develop in regions where there are separations from unidirectional laminar blood flow, typically near branches, bifurcations, regions of arterial narrowing, and curvatures in the arteries (1, 2). Obviously, homodynamic forces play a key role in atherosclerosis. Studies also indicate that vascular endothelium function disturbance, especially impairment of endothelium dependent vasodilation, is involved (3). Shear stress affects endothelial cells in many ways, such as cytoskeletal rearrangement, decrease of intracellular pH, release of PGI2 and some growth factors (PDGF, FGF, ECGF, TGF-b, etc), activation of IP3 and mitogen-activated protein kinases, and the significant increase in the production of nitric oxide (1,2,4,5). As an important function factor of vascular endothelial cells, nitric oxide (NO) is closely related to the endothelial dysfunction and atherosclerosis (6). Endothelial derived nitric oxide involves in many events in the vasculature, including vasodilation, inhibition of platelet aggregation, adhesion molecule expression, and vascular smooth muscle proliferation, which are directly or indirectly related to atherosclerosis. Endothelial cells release NO more potently in response to increased shear stress than to agonists that raise intracellular free calcium concentration [Ca2+]i. Studies have indicated that NO production increases with a calcium/CaM dependent manner in the first few minutes after exposed to shear stress, followed by a sustained NO production that occurs more than 30min which is Ca2+ independent (7). The activation of eNOS by shear stress, which modulated by Ca/CaM, G protein, tyrosine kinase phosphorylation and eNOS gene expression, is responsible for the increase of NO production (8). However, the contribution of extracellular calcium to the production of NO is somewhat contradictory.
2
Abdelsalam, Shahenda Salaheldine, and Abdelali Agouni. "Protein Tyrosine Phosphatase (PTP) 1B Inhibition Improves Endoplasmic Reticulum Stress-Induced Apoptosis and Impaired Angiogenic Response in Endothelial Cells." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0110.
Full textAbstract:
Insulin is not only important for glucose homeostasis, but also plays a critical role in the activation of endothelial nitric oxide synthase (eNOS) to synthesize nitric oxide (NO) and keeping the endothelium functional. Conditions which result in insulin resistance, such as diabetes and obesity, cause impairment of endothelial function, a condition known as endothelial dysfunction that features a reduced release of NO. Protein tyrosine phosphatase (PTP) 1B, is a known negative regulator of insulin receptor, that has been implicated in the pathogenesis of insulin resistance and endothelial dysfunction. Owing to its critical location at the surface of the endoplasmic reticulum (ER), PTP1B has been found to play an important role in ER stress response. However, the role of ER stress in PTP1B-mediated endothelial dysfunction is not fully elucidated. Toa address this, ER stress was induced pharmacologically in endothelial cells using thapsigargin, in the presence or absence of either a small molecule inhibitor of PTP1B or silencing siRNA duplexes, followed by the assessment of the expression of key ER stress markers, angiogenic capacity and apoptotic signals. We report here, that PTP1B inhibition protected cells against ER stress and ER stress-induced impairment in eNOS activation and angiogenic capacity. PTP1B inhibition or silencing also protected against ER stress-induced endothelial cell apoptosis. Moreover, PTP1B blockade also suppressed ER stress-activated autophagy. Our data emphasize on the critical role of PTP1B in ER stress-mediated endothelial cell dysfunction and highlights the therapeutic potential of PTP1B inhibition against ER stress-mediated cell death and impairment of endothelial function to prevent cardiovascular disease in pathologies charactereized by the activation of ER stress such as diabetes.
3
Kant, Nimita, and Perumal Senthiappan Jayaraj. "Evaluation of Telomerase Reverse Transcriptase Expression in Squamous Cell Carcinoma of the Skin." In Annual Conference of Indian Society of Medical and Paediatric Oncology (ISMPO). Thieme Medical and Scientific Publishers Pvt. Ltd., 2021. http://dx.doi.org/10.1055/s-0041-1735375.
Full textAbstract:
Abstract Introduction Squamous cell carcinoma (SCC) is highly invasive malignant tumor showing keratinocytic differentiation and is often associated with chronic exposure to UV light. Telomerase is RNA dependent DNA polymerase that causes addition of telomeric repeat DNA sequences to chromosomal ends. Recently, UV signature mutations have been identified in core promoter region of TERT gene, which encodes the main catalytic subunit leading to overexpression in cutaneous melanoma. However, its role and expression pattern have not been studied in eyelid skin SCC. Objectives Present study aimed to analyze the presence of telomerase reverse transcriptase (TERT) in eyelid SCC, as its expression pattern and mutational status have not been studied in SCC. Materials and Methods Nineteen cases of eyelid SCC were evaluated for the presence of TERT protein using monoclonal antibody against TERT, and its mutational status was verified using PCR and DNA sequencing. Bioedit software was used for analyzes and primers were vindicated using NCBI Primer Blast. Results were correlated with clinicopathological features of SCC. Results A C to T mutation was observed in 6 of 19 SCC cases. Positive expression of TERT was found in 57% of the cases analyzed and it showed a significant association with keratinocytic differentiation (p = 0.04). Conclusion Relation between TERT promoter mutation and TERT immunohistochemistry is studied for the first time in eyelid skin SCC. Our results suggested that overexpression of TERT may contribute to the aggressive behavior associated with SCC and such patients may warrant aggressive treatment.