期刊
MOLECULAR AND CELLULAR BIOCHEMISTRY
卷 461, 期 1-2, 页码 119-126出版社
SPRINGER
DOI: 10.1007/s11010-019-03595-8
关键词
IL-6; TGF-beta 2; STAT3; Cell survival; Apoptosis
类别
资金
- National Natural Science Foundation of China [31571439]
- Qingdao Scientific and Technological Innovation center for Marine Biomedicine Development Grant [2017-CXZX01-2-2]
- Ocean University of China
Transforming growth factor beta is a key cytokine involved in the pathogenesis of fibrosis in many organs, whereas interleukin-6 plays an important role in the regulation of inflammation. They are both potent angiogenesis inducers with opposite effects on cell survival and apoptosis. TGF-beta 2 induces apoptosis; in contrast, IL-6 protects cells from apoptosis. The possible interaction between these two cytokines is indicated in various disease states. In this study, we have assessed the effect of TGF-beta 2 on IL-6 signaling and found that TGF-beta 2 could strongly inhibit IL-6-induced STAT3 activation and synergy with IL-6 resulting in enhanced SOCS3 expression. Interestingly, IL-6 also slows down the decay of TGF-beta 2 mRNA. Consistent with this mechanism, we found that TGF-beta 2 could antagonize IL-6 effect on cell survival in both gamma-irradiation and UV light-induced apoptosis. Taken together, the finding shows that TGF-beta 2 serves as a negative regulator of IL-6 signaling and antagonizes the anti-apoptosis effect of IL-6.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据