کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8477250 | 1550895 | 2014 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Mitogen-activated protein kinases and protein phosphatase 5 mediate glucocorticoid-induced cytotoxicity in pancreatic islets and β-cells
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کلمات کلیدی
SB203580PP5T2DMDEXASP600125eIF2αUPRRU486ASK-1Jnkc-Jun N-terminal kinase - C-Jun N-terminal kinaseMAPK - MAPKp38 MAPK - P38 MAPKROS - ROSPancreatic islet - جزیره پانکراسApoptosis - خزان یاختهایDexamethasone - دگزامتازونType 2 diabetes mellitus - دیابت نوع دوeukaryotic translation initiation factor 2α - عامل آغازگر ترجمه یوکاریوتی 2αUnfolded protein response - پاسخ پروتئین آشکارprotein phosphatase 5 - پروتئین فسفاتاز 5mitogen-activated protein kinase - پروتئین کیناز فعال با mitogenapoptosis signal-regulating kinase 1 - کیناز تنظیم کننده سیگنال آپوپتوز 1Glucocorticoid - گلوکوکورتیکوئیدهاGlucocorticoids - گلوکوکورتیکوئیدهاReactive oxygen species - گونههای فعال اکسیژنglucocorticoid receptor - گیرنده گلوکوکورتیکوئید
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Mitogen-activated protein kinases and protein phosphatase 5 mediate glucocorticoid-induced cytotoxicity in pancreatic islets and β-cells Mitogen-activated protein kinases and protein phosphatase 5 mediate glucocorticoid-induced cytotoxicity in pancreatic islets and β-cells](/preview/png/8477250.png)
چکیده انگلیسی
Glucocorticoid excess is associated with glucose intolerance and diabetes. In addition to inducing insulin resistance, glucocorticoids impair β-cell function and cause β-cell apoptosis. In this study we show that dexamethasone activates mitogen-activated protein kinases (MAPKs) signaling in MIN6 β-cells, as evident by enhanced phosphorylation of p38 MAPK and c-Jun N-terminal kinase (JNK). In contrast, the integrated stress response pathway was inhibited by dexamethasone. A p38 MAPK inhibitor attenuated dexamethasone-induced apoptosis in β-cells and isolated islets and decreased glucocorticoid receptor phosphorylation at S220. In contrast, a JNK inhibitor augmented DNA fragmentation and dexamethasone-induced formation of cleaved caspase 3. We also show that inhibition of protein phosphatase 5 (PP5) augments apoptosis in dexamethasone-exposed islets and β-cells, with a concomitant activation of p38 MAPK. In conclusion, our data provide evidence that in islets and β-cells, p38 MAPK and JNK phosphorylation work in concert with PP5 to regulate the cytotoxic effects exerted by glucocorticoids.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Endocrinology - Volume 383, Issues 1â2, 5 March 2014, Pages 126-136
Journal: Molecular and Cellular Endocrinology - Volume 383, Issues 1â2, 5 March 2014, Pages 126-136
نویسندگان
Liselotte Fransson, Victoria Rosengren, Titu Kumar Saha, Nina Grankvist, Tohidul Islam, Richard E. Honkanen, Ã
ke Sjöholm, Henrik Ortsäter,