| Autor: |
Du, Yuping, Sun, Jingjie, Liu, Xinning, Nan, Jing, Qin, Xiaodong, Wang, Xiao, Guo, Jihui, Zhao, Chenyang, Yang, Jinbo |
| Zdroj: |
Molecular & Cellular Biochemistry; Nov2019, Vol. 461 Issue 1/2, p119-126, 8p |
| Abstrakt: |
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-β2 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-β2 on IL-6 signaling and found that TGF-β2 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-β2 mRNA. Consistent with this mechanism, we found that TGF-β2 could antagonize IL-6 effect on cell survival in both γ-irradiation and UV light-induced apoptosis. Taken together, the finding shows that TGF-β2 serves as a negative regulator of IL-6 signaling and antagonizes the anti-apoptosis effect of IL-6. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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