Growth differentiation factor 11 inhibits adipogenic differentiation by activating TGF-beta/Smad signalling pathway

Growth differentiation factor 11 inhibits adipogenic differentiation by activating TGF-beta/Smad signalling pathway
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生长分化因子 11 通过激活 TGF-β/Smad 信号通路抑制脂肪形成分化

DOI:
10.1111/cpr.12631
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发表时间:
2019-07-01
期刊:
影响因子:
8.5
通讯作者:
Liu, Weiqing
Liu, Weiqing
中科院分区:
生物学1区
文献类型:
--
作者:
Luo, Hongke;Guo, Yuchen;Liu, Weiqing

文献摘要

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Objectives Growth differentiation factor 11 (GDF11), an emerging secreted member of the TGF-beta superfamily, plays essential roles in development, physiology and multiple diseases; however, its role during adipogenic differentiation and the underlying mechanisms remains poorly understood. Materials and methods Bone marrow-derived human mesenchymal stem cells (hMSCs) and 3T3-L1 pre-adipocytes were induced with adipogenic culture medium supplementing with different concentrations of recombinant GDF11 (rGDF11 0, 10, 50, 100 ng mL(-1)). Oil Red O staining, qRT-PCR analysis, Western blot analysis and immunofluorescence staining were performed to assay adipogenesis. Results For both hMSCs and 3T3-L1 pre-adipocytes, the presence of rGDF11 leads to a dose-dependent reduction of intracellular lipid droplet accumulation and suppressed adipogenic-related gene expression. Mechanically, GDF11 inhibits adipogenesis by activating Smad2/3-dependent TGF-beta signalling pathway, and these inhibitory effects could be restored by SB-431542, a pharmacological TGF-beta type I receptor inhibitor. Conclusions Taken together, our data indicates that GDF11 inhibits adipogenic differentiation in both hMSCs and 3T3-L1 pre-adipocytes by activating Smad2/3-dependent TGF-beta signalling pathway.