کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9879429 | 1534758 | 2005 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Bigendothelin-1 via p38-MAPK-dependent mechanism regulates adult rat ventricular myocyte contractility in sepsis
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کلمات کلیدی
ECE-1NOS2SIRSKHBTBSTD5WChFET-1IL-10i.p.CLPARVMPVDFJnkSDSM199LPSc-Jun N-terminal kinase - C-Jun N-terminal kinaseERK1/2 - ERK1 / 2MAPK - MAPKMitogen activated protein kinases - Mitogen فعال پروتئین کینازBig endothelin-1 - اندوتلین بزرگ 1endothelin-1 - اندوتلین-1Cecal ligation and puncture - انقباض و سوراخ شدن سکته مغزیInterleukin-10 - اینترلوکین 10Immunoblot analysis - تجزیه و تحلیل ایمونولوژیکanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of varianceintraperitoneal - داخل صفاقیpolyvinylidene difluoride - دی فلوئورید پلی وینیلیدینsodium dodecyl sulfate - سدیم دودسیل سولفاتSystemic inflammatory response syndrome - سندرم پاسخ سیستماتیک التهابیShr - شریlipopolysaccharide - لیپوپلی ساکاریدmedium 199 - متوسط 199Spontaneously hypertensive rats - موش های خودبخود فشار خون بالاadult rat ventricular myocytes - میوکسی های بطنی بالغ رتChronic heart failure - نارسایی مزمن قلبیNitric oxide - نیتریک اکسیدextracellular signal-regulated kinase 1 and 2 - کیناز 1 و 2 تنظیم شده با سیگنال خارج سلولی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
We tested the hypothesis that exogenous administration of the ET-1 precursor, bigET-1, would regulate adult rat ventricular myocyte (ARVM) contractility in a p38-mitogen activated protein kinase (p38-MAPK)-dependent mechanism during sepsis. Ventricular myocytes from adult rat hearts (both sham and septic) were stimulated to contract at 0.5 Hz and mechanical properties were evaluated using an IonOptix Myocam system. Immunoblot analysis was used to determine the phosphorylation of p38-MAPK and extracellular signal-regulated kinase 1/2 (ERK1/2). ARVMs were treated with vehicle, bigET-1 and inhibitors for 24 h and then subjected to functional and biochemical estimations. Septic ARVM displayed a distorted cell membrane and irregular network within the cells along with increased cell contractility as evidenced by elevated peak shortening (PS), maximal velocity of shortening (+dL/dt) and relengthening (âdL/dt) in comparison to sham ARVM. BigET-1 treatment caused ARVM enlargement in both sham and sepsis groups. BigET-1 (100 nM) produced an increase in ARVM contractility in sham group as compared to vehicle treatment. However, septic ARVM treated with bigET-1 exhibited unaltered ARVM contractility, and upregulated ETB receptors as compared to respective sham group. BigET-1 increased the concentration of ET-1 and upregulated phosphorylation of p38-MAPK but not of ERK1/2 in sham and septic ARVM. Furthermore, inhibition of p38-MAPK by SB203580 (10 μM) increased ARVM contractility in sham but not in sepsis group. BigET-1 reversed SB203580-induced increase in PS in sham group but accentuated it in sepsis group. BigET-1 also reversed SB203580-induced inhibition of p38-MAPK phosphorylation in sham but not in septic ARVM. SB203580 pretreatment followed by bigET-1 administration significantly decreased p38-MAPK phosphorylation and downregulated ETB receptor expression as compared to bigET-1 treatment per se in sepsis group but not in sham. We concluded that a bigET-1-induced non-responsive effect on septic ARVM contractile function could be due to upregulation of p38-MAPK phosphorylation and ETB receptor expression.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1741, Issues 1â2, 30 June 2005, Pages 127-139
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1741, Issues 1â2, 30 June 2005, Pages 127-139
نویسندگان
Akanksha Gupta, Nicholas S. II, Ruchita Kapoor, Jun Ren, Avadhesh C. Sharma,