Effect of suppressor of cytokine signaling 2 (SOCS2) on fat metabolism induced by growth hormone (GH) in porcine primary adipocyte
Effect of suppressor of cytokine signaling 2 (SOCS2) on fat metabolism induced by growth hormone (GH) in porcine primary adipocyte
复制标题
细胞因子信号传导抑制因子2（SOCS2）对生长激素（GH）诱导的猪原代脂肪细胞脂肪代谢的影响
DOI：
10.1007/s11033-012-1783-9
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发表时间：
2012-09-01
影响因子：
2.8
通讯作者：
Qi, Ren Li
中科院分区：
文献类型：
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作者：
Yang, Hai Li;Sun, Chan;Qi, Ren Li
SOCS2 是细胞因子信号传导抑制因子 (SOCS) 家族的成员，是信号通路 Janus 激酶/信号转导器和转录激活子 (JAK/STAT) 的负调节因子。生长激素（GH）可以刺激脂肪组织中的脂肪分解。为了证明 SOCS2 对 GH 诱导的猪脂肪细胞分化和脂质代谢的具体影响，我们用 500 ng/ml GH 诱导猪原代脂肪细胞，然后测试脂质代谢中关键基因的甘油三酯 (TG) 积累和 mRNA 表达，如过氧化物酶体增殖物激活受体 γ (PPARγ)、脂肪酸合酶 (FAS)、脂肪甘油三酯脂肪酶 (ATGL)、激素敏感脂肪酶 (HSL)、SOCS2 和 SOCS3。然后，我们在原代脂肪细胞中过度表达 SOCS2 并用 500 ng/ml GH 处理后，在不同时间点重新测试这些基因的表达。结果显示，500 ng/ml GH 显着抑制猪原代脂肪细胞的分化。具体来说，GH诱导后0.5小时，TG积累开始增加，8小时后开始下降。 GH在早期(0-1 h)可以促进PPARγ和FAS的表达，从4 h开始抑制。而ATGL和HSLmRNA表达量则稳定增加。 GH刺激后SOCS2的表达稳定增加，而SOCS3的表达瞬时上升。 SOCS2的过表达显着降低了GH诱导的早期（0-1小时）PPARγ、FAS、ATGL和HSL mRNA表达的增加，以及FAS和ATGL蛋白的表达。另外，SOCS2 过表达显着降低了 GH 刺激下的信号转导器和转录激活剂 3 (STAT3)、信号转导器和转录激活剂 5 (STAT5) mRNA 表达以及酪氨酸磷酸化水平。同时Ad-SOCS2转染的脂肪细胞中SOCS3mRNA保持在较低水平。总之，SOCS2可能是猪脂肪细胞GH信号的重要负调节因子，这为SOCS2调节脂肪代谢的机制提供了基础。
SOCS2, a member of suppressor of cytokine signaling (SOCS) family, is a negative regulator of the signal pathway Janus kinase/signal transducers and activators of transcription (JAK/STAT). Growth hormone (GH) could stimulate lipolysis in adipose tissue. To demonstrate the specific influence ofSOCS2on porcine adipocytes differentiation and lipid metabolism induced by GH, we induced porcine primary adipocytes with 500 ng/ml GH and then tested the triglyceride (TG) accumulation and mRNA expressions of crucial genes in lipid metabolism like peroxisome proliferator-activated receptor gamma (PPARγ), fatty acid synthase (FAS), adipose triglyceride lipase (ATGL), hormone-sensitive lipase (HSL),SOCS2andSOCS3. Then we retested these genes expressions in different time point after further treatment that over expressedSOCS2in primary adipocytes and treated with 500 ng/ml GH. Results showed 500 ng/ml GH significantly restrained the porcine primary adipocytes differentiation. Specifically, 0.5 h after the induction with GH, accumulation of TG began to increase, and turned down since 8 h after. GH could promotePPARγandFASexpressions during earlier stage (0–1 h), restrain from 4 h. However,ATGLandHSLmRNA expressions were stabile increasing. The expression ofSOCS2increased steadily after GH stimulation whileSOCS3expression was instantaneous rise. Overexpression ofSOCS2significantly decreased GH-induced the increase ofPPARγ,FAS,ATGLandHSLmRNA expressions in earlier stage (0–1 h), as well asFASandATGLprotein expression. OtherwiseSOCS2overexpression significantly decreased signal transducers and activators of transcription 3 (STAT3), signal transducers and activators of transcription 5 (STAT5) mRNA expressions and tyrosine phosphorylation levels with GH stimulation. At the same timeSOCS3mRNA kept in a lower level in Ad-SOCS2transfected adipocytes. In conclusion,SOCS2might be an important negative regulator of GH signaling in porcine adipocytes, which would provide the ground work for the mechanism of SOCS2 regulation fat metabolism.