کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8337359 | 1540671 | 2013 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Myocardium proteome remodelling after nutritional deprivation of methyl donors
ترجمه فارسی عنوان
بازسازی پروتئین میوکارد پس از محرومیت از اهداکنندگان مکمل
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کلمات کلیدی
sHSPPPARMDDIPAPGC-1αDTTDNPHHcy2-DFBSHHcyPTM2,4-dinitrophenylhydrazine - 2،4-dinitrophenylhydrazinepost-translational modification - اصلاح post-translationalmethyl donor - اهدا کننده متیلCardiovascular diseases - بیماری قلبی-عروقی Ingenuity Pathway Analysis - تجزیه و تحلیل راه Ingenuityfold change - تغییر در برابرTwo-dimension - دو بعدیdithiothreitol - دیتیوتریتولCVD - رسوب دهی شیمیایی بخار fetal bovine serum - سرم جنین گاوH9c2 cells - سلول های H9c2Mass spectrometry - طیف سنجی جرمیMyocardium - میوکارد Isoelectric point - نقطه ایزوالکتریکhomocysteine - هوموسیستئینHyperhomocysteinemia - هیپر هوموسایستنمیMolecular weight - وزن مولکولیProteomics - پروتئومیکسsmall heat shock protein - پروتئین شوک حرارتی کوچکCHAPS - چاپسprotein carbonyl - کربونیل پروتئینControl - کنترلperoxisome proliferator-activated receptor - گیرنده فعال فعال پروکسیوم
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
چکیده انگلیسی
Methyl donor (MD: folate, vitamin B12 and choline) deficiency causes hyperhomocysteinemia, a risk factor for cardiovascular diseases. However, the mechanisms of the association between MD deficiency, hyperhomocysteinemia, and cardiomyopathy remain unclear. Therefore, we performed a proteomic analysis of myocardium of pups from rat dams fed a MD-depleted diet to understand the impact of MD deficiency on heart at the protein level. Two-dimension gel electrophoresis and mass spectrometry-based analyses allowed us to identify 39 proteins with significantly altered abundance in MD-deficient myocardium. Ingenuity Pathway Analysis showed that 87% of them fitted to a single protein network associated with developmental disorder, cellular compromise and lipid metabolism. Concurrently increased protein carbonylation, the major oxidative post-translational protein modification, could contribute to the decreased abundance of many myocardial proteins after MD deficiency. To decipher the effect of MD deficiency on the abundance of specific proteins identified in vivo, we developed an in vitro model using the cardiomyoblast cell line H9c2. After a 4-day exposure to a MD-deprived (vs. complete) medium, cells were deficient of folate and vitamin B12, and released abnormal amounts of homocysteine. Western blot analyses of pup myocardium and H9c2 cells yielded similar findings for several proteins. Of specific interest is the result showing increased and decreased abundances of prohibitin and α-crystallin B, respectively, which underlines mitochondrial injury and endoplasmic reticulum stress within MD deficiency. The in vitro findings validate the MD-deficient H9c2 cells as a relevant model for studying mechanisms of the early metabolic changes occurring in cardiac cells after MD deprivation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The Journal of Nutritional Biochemistry - Volume 24, Issue 7, July 2013, Pages 1241-1250
Journal: The Journal of Nutritional Biochemistry - Volume 24, Issue 7, July 2013, Pages 1241-1250
نویسندگان
Emilie Martinez, Nicolas Gérard, Maira M. Garcia, Andrzej Mazur, Rosa-Maria Guéant-Rodriguez, Blandine Comte, Jean-Louis Guéant, Patrick Brachet,