کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5504345 | 1536276 | 2017 | 17 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The nitroxide 4-methoxy TEMPO inhibits neutrophil-stimulated kinase activation in H9c2 cardiomyocytes
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کلمات کلیدی
fMLPMMPPTPHOClAmI - AMIMPO - DFOMAPK - MAPKinflammation - التهاب( توروم) coronary artery disease - بیماری عروق کرونرTyr - تیرTyrosine - تیروزینApoptosis - خزان یاختهایAcute myocardial infarction - سکته قلبیCAD - طراحی به کمک رایانه یا کَدPlatelet activating factor - عامل فعال کننده پلاکتFormyl-methionyl-leucyl-phenylalanine - فرمول متیونیل-لوسیل-فنیل آلانینmatrix metalloproteinase - ماتریکس متالوپروتئینازmyeloperoxidase - میلوپراکسیداز myocyte - میوسیتneutrophil - نوتروفیلPAF - نیروی هوایی پاکستانProtein tyrosine phosphatase - پروتئین تیروزین فسفاتازMAP kinase - کیناز MAPmitogen-activated protein kinases - کیناز پروتئین فعال Mitogen
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
After acute myocardial infarction (AMI), neutrophils are recruited to the affected myocardium. Hypochlorous acid (HOCl) produced by neutrophil myeloperoxidase (MPO) damages cardiomyocytes and potentially expands the primary infarct. Rat cardiomyocyte-like cells were incubated with isolated human neutrophils treated with chemical activators in the absence or presence of nitroxide 4-methoxy-Tempo (MetT; 25 μM) for 4, 6 or 24 h; studies with reagent HOCl served as positive control. Treating cardiomyocytes with activated neutrophils or reagent HOCl resulted in a marked increase in protein tyrosine chlorination and a decline in protein tyrosine phosphatase (PTP) activity. On balance our data also supported an increase in phosphorylation of MAPK p38 and ERK1/2 suggestive of an intracellular hyperphosphorylation status and this was accompanied by decreases in cell viability, as judged by assessing caspases-3/7 activity. For cells exposed to activated neutrophils receptor-mediated uptake of transferrin decreased although total matrix metalloproteinase (MMP) activity was unaffected. Addition of MetT ameliorated protein tyrosine chlorination, decreased MAPK activity and restored receptor-mediated transferrin uptake and PTP activity in cardiomyocytes. Overall, adverse effects of neutrophil-derived HOCl on cultured cardiomyocytes were ameliorated by MetT suggesting that nitroxides may be beneficial to inflammatory pathologies, where neutrophil recruitment/activation is a prominent and early feature.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Archives of Biochemistry and Biophysics - Volume 629, 1 September 2017, Pages 19-35
Journal: Archives of Biochemistry and Biophysics - Volume 629, 1 September 2017, Pages 19-35
نویسندگان
B. Chami, G. Jeong, A. Varda, A.-M. Maw, H.-B. Kim, G.M. Fong, M. Simone, B.S. Rayner, X.-S. Wang, J.M. Dennis, P.K. Witting,