S-NITROSOGLUTATHIONE REDUCTASE KNOCKOUT MICE PREVENT POST-MYOCARDIAL INFARCTION IMPAIRMENT OF CALCIUM REUPTAKE
نویسندگان
چکیده
منابع مشابه
S-Nitrosoglutathione Reductase Deficiency Enhances the Proliferative Expansion of Adult Heart Progenitors and Myocytes Post Myocardial Infarction
BACKGROUND Mammalian heart regenerative activity is lost before adulthood but increases after cardiac injury. Cardiac repair mechanisms, which involve both endogenous cardiac stem cells (CSCs) and cardiomyocyte cell-cycle reentry, are inadequate to achieve full recovery after myocardial infarction (MI). Mice deficient in S-nitrosoglutathione reductase (GSNOR(-⁄-)), an enzyme regulating S-nitros...
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Myocardial depression is an important contributor to morbidity and mortality in septic patients. Nitric oxide (NO) plays an important role in the development of septic cardiomyopathy, but also has protective effects. Recent evidence has indicated that NO exerts many of its downstream effects on the cardiovascular system via protein S-nitrosylation, which is negatively regulated by S-nitrosoglut...
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NO is critical to immunity, but its role in the development of the immune system is unknown. In this study, we show that S-nitrosoglutathione reductase (GSNOR), a protein key to the control of protein S-nitrosylation, is important for the development of lymphocytes. Genetic deletion of GSNOR in mice results in significant decrease in both T and B lymphocytes in the periphery. In thymus, GSNOR d...
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S-nitrosoglutathione (GSNO) is considered a natural nitric oxide (NO.) reservoir and a reactive nitrogen intermediate in animal cells, but little is known about this molecule and its metabolism in plant systems. In this work, using pea plants as a model system, the presence of GSNO in collenchyma cells was demonstrated by an immunohistochemical method. When pea plants were grown with a toxic Cd...
متن کاملHuman carbonyl reductase 1 is an S-nitrosoglutathione reductase.
Human carbonyl reductase 1 (hCBR1) is an NADPH-dependent short chain dehydrogenase/reductase with broad substrate specificity and is thought to be responsible for the in vivo reduction of quinones, prostaglandins, and other carbonyl-containing compounds including xenobiotics. In addition, hCBR1 possesses a glutathione binding site that allows for increased affinity toward GSH-conjugated molecul...
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ژورنال
عنوان ژورنال: Journal of the American College of Cardiology
سال: 2012
ISSN: 0735-1097
DOI: 10.1016/s0735-1097(12)61393-x