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学科主题: 基础医学
题名:
Suppressor of cytokine signaling 1 protects rat pancreatic islets from cytokine-induced apoptosis through Janus kinase/signal transducers and activators of transcription pathway
作者: Sun Qi1; Xiang Ruo-lan3; Yang Yan-li2; Feng Kai1; Zhang Kui1; Ding Wen-yi1
关键词: pancreatic beta-cell ; cytokine ; apoptosis ; SOCS1 ; JAK/STAT
刊名: CHINESE MEDICAL JOURNAL
发表日期: 2013-11-05
DOI: 10.3760/cma.j.issn.0366-6999.20130557
卷: 126, 期:21, 页:4048-4053
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Medicine, General & Internal
研究领域[WOS]: General & Internal Medicine
关键词[WOS]: BETA-CELL APOPTOSIS ; IFN-GAMMA ; AUTOIMMUNE DESTRUCTION ; GENE-EXPRESSION ; JAK/STAT ; SOCS1 ; OVEREXPRESSION ; MODULATION ; IL-1-BETA ; ALPHA
英文摘要:

Background Suppressor of cytokine signaling (SOCS) proteins are inhibitors of cytokine signaling pathway involved in negative feedback loops. Although SOCS1 is an important intracellular suppressor of apoptosis in a variety of cell types, its role in cytokine-induced pancreatic beta-cell apoptosis remains unclear. The present study investigated potential effects of SOCS1 on the cytokine-induced pancreatic beta-cell apoptosis.

Methods After successfully transfected with SOCS1/pEGFP-C1 or pEGFP-C1 plasmids to overexpress SOCS1, RINm5F (rat insulinoma cell line) cells were exposed to cytokines, interferon (IFN)-gamma alone, IFN-gamma+interleukin (IL)-1 beta, IFN-gamma+IL-1 beta+ tumor necrosis factor (TNF)-alpha respectively. Pancreatic beta-cell apoptosis was assessed by using MTT, FACS, and caspase-3 activity assays. Protein phosphorylation of Janus kinase 2 (JAK2) and signal transducers and activators of transcription 1 (STAT1) were verified by Western blotting and mRNA expression of inducible nitric oxide synthase (iNOS), NF-kappa beta and Fas were analyzed by RT-PCR.

Results Overexpression of SOCS1 in RINm5F cells was shown to attenuate IFN-gamma alone, IFN-gamma+IL-1 beta and IFN-gamma+TNF-alpha+IL-1 beta mediated apoptosis. Phosphorylation of JAK2 and STAT1 significantly decreased in RINm5F cells which overexpressed SOCS1 protein. Overexpression of SOCS1 significantly suppressed cytokine-induced iNOS mRNA levels.

Conclusion Overexpression of SOCS1 protects pancreatic islets from cytokine-induced cell apoptosis via the JAK2/STAT1 pathway.

语种: 英语
所属项目编号: 7082076
项目资助者: Natural Science Foundation of Beijing ; National Key Program of Clinical Science
WOS记录号: WOS:000327916400009
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内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/67708
Appears in Collections:基础医学院_期刊论文

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作者单位: 1.Chinese Acad Med Sci, Peking Union Med Coll Hosp, Minist Hlth, Dept Endocrinol,Key Lab Endocrinol, Beijing 100730, Peoples R China
2.Chinese Acad Med Sci, Peking Union Med Coll Hosp, Dept Internal Med, Beijing 100730, Peoples R China
3.Peking Univ, Hlth Sci Ctr, Sch Basic Med Sci, Dept Physiol & Pathophysiol,Key Lab Mol Cardiovas, Beijing 100191, Peoples R China

Recommended Citation:
Sun Qi,Xiang Ruo-lan,Yang Yan-li,et al. Suppressor of cytokine signaling 1 protects rat pancreatic islets from cytokine-induced apoptosis through Janus kinase/signal transducers and activators of transcription pathway[J]. CHINESE MEDICAL JOURNAL,2013,126(21):4048-4053.
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