کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10738553 | 1046714 | 2011 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Nox4 regulates Nrf2 and glutathione redox in cardiomyocytes in vivo
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کلمات کلیدی
PAGEMLC2vα myosin heavy chainαMHCβMHCNOX4ECLNADPHNrf2PBSDTTPVDFq-PCR - Q-PCRpolyacrylamide gel electrophoresis - الکتروفورز ژل پلی آکریل آمیدenhanced chemiluminescence - بهبود شیمیایی لومنReverse transcriptase - ترانس کریپتاز معکوس یا وارونویسELISA - تست الیزاembryoid body - جنین جنینstandard error of the mean - خطای استاندارد میانگینpolyvinylidene difluoride - دی فلوئورید پلی وینیلیدینdithiothreitol - دیتیوتریتولendoplasmic reticulum - شبکه آندوپلاسمی NF-E2-related factor 2 - عامل NF-E2 2Cardiomyocytes - قلب و عروقPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریSEM - مدل معادلات ساختاری / میکروسکوپ الکترونی روبشیnicotinamide adenine dinucleotide phosphate - نیکوتین آمید adenine dinucleotide phosphatequantitative polymerase chain reaction - واکنش زنجیره ای پلیمراز کمیGlutathione - گلوتاتیونReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Nox4 regulates Nrf2 and glutathione redox in cardiomyocytes in vivo Nox4 regulates Nrf2 and glutathione redox in cardiomyocytes in vivo](/preview/png/10738553.png)
چکیده انگلیسی
NADPH oxidase-4 (Nox4) is an important modulator of redox signaling that is inducible at the level of transcriptional expression in multiple cell types. By contrast to other Nox enzymes, Nox4 is continuously active without requiring stimulation. We reported recently that expression of Nox4 is induced in the adult heart as an adaptive stress response to pathophysiological insult. To elucidate the potential downstream target(s) regulated by Nox4, we performed a microarray screen to assess the transcriptomes of transgenic (tg) mouse hearts in which Nox4 was overexpressed. The screen revealed a significant increase in the expression of many antioxidant and detoxifying genes regulated by Nrf2 in tg compared to wild-type (wt) mouse hearts, and this finding was subsequently confirmed by Q-PCR. Expression of glutathione biosynthetic and recycling enzymes was increased in tg hearts and associated with higher levels of both GSH and the ratio of reduced:oxidised GSH, compared to wt hearts. The increases in expression of the antioxidant genes and the changes in glutathione redox effected by Nox4 were ablated in an Nrf2-null genetic background. These data therefore demonstrate that Nox4 can activate the Nrf2-regulated pathway, and suggest a potential role for Nox4 in the regulation of GSH redox in cardiomyocytes.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 51, Issue 1, 1 July 2011, Pages 205-215
Journal: Free Radical Biology and Medicine - Volume 51, Issue 1, 1 July 2011, Pages 205-215
نویسندگان
Alison C. Brewer, Thomas V.A. Murray, Matthew Arno, Min Zhang, Narayana P. Anilkumar, Giovanni E. Mann, Ajay M. Shah,