کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1964300 | 1058540 | 2007 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Ethanol induces apoptosis in hepatocytes by a pathway involving novel protein kinase C isoforms
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کلمات کلیدی
NF-κBDAPIAP-1MnTBAPPKCERK1/2 - ERK1 / 2JNK1/2 - JNK1 / 2MAPK - MAPKALD - آدرنولکودیستروفیelectromobility shift assay - آزمایش الکتریکی حرکتیTranslocation - انتقالalcoholic liver disease - بیماری کبدی الکلیTdT-mediated dUTP nick end labeling - تلگراف پایان نام نهایی DUTP TdTOxidative stress - تنش اکسیداتیوTUNEL - تونلApoptosis - خزان یاختهایEMSA یا electrophoretic mobility shift assay - سنجش تغییر تحرک الکتروفورتیکnuclear factor kappa B - فاکتور هسته ای کاپا BPhosphorylation - فسفریلاسیونPrimary rat hepatocytes - هپاتوسیتهای مویرگی اولیهactivator protein-1 - پروتئین فعال کننده-1Protein kinase C - پروتئین کیناز سیmitogen-activated protein kinase - پروتئین کیناز فعال با mitogen
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Ethanol abuse is one of the major etiologies of cirrhosis. Ethanol has been shown to induce apoptosis via activation of oxidative stress, mitogen-activated protein kinases (MAPK), and tyrosine kinases. However, there is a paucity of data that examine the interplay among these molecules. In the present study we have systematically elucidated the role of novel protein kinase C isoforms (nPKC; PKCδ and PKCÉ) in ethanol-induced apoptosis in hepatocytes. Ethanol enhanced membrane translocation of PKCδ and PKCÉ, which was associated with the phosphorylation of p38MAPK, p42/44MAPK and JNK1/2, and the nuclear translocation of NF-κB and AP-1. This resulted in increased apoptosis in primary rat hepatocytes. Inhibition of both PKCδ and PKCÉ resulted in a decreased MAPK activation, decreased nuclear translocation of NF-κB and AP-1, and inhibition of apoptosis. In addition, ethanol activated the tyrosine phosphorylation of PKCδ via tyrosine kinase in hepatocytes. The tyrosine phosphorylated PKCδ was cleaved by caspase-3 and these fragments were translocated to the nucleus. Inhibition of ethanol-induced oxidative stress blocked the membrane translocation of PKCδ and PKCÉ, and the tyrosine phosphorylation of PKCδ in hepatocytes. Inhibition of oxidative stress, tyrosine kinase or caspase-3 activity caused a decreased nuclear translocation of PKCδ in response to ethanol, and was associated with less apoptosis. Conclusion: These results provide a newly-described mechanism by which ethanol induces apoptosis via activation of nPKC isoforms in hepatocytes.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cellular Signalling - Volume 19, Issue 11, November 2007, Pages 2339-2350
Journal: Cellular Signalling - Volume 19, Issue 11, November 2007, Pages 2339-2350
نویسندگان
Yanhong Zhang, Senthil K. Venugopal, Songqing He, Pingguo Liu, Jian Wu, Mark A. Zern,