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首页> 外文期刊>Cellular Physiology and Biochemistry >Rapamycin Promotes the Survival and Adipogenesis of Ischemia-Challenged Adipose Derived Stem Cells by Improving Autophagy
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Rapamycin Promotes the Survival and Adipogenesis of Ischemia-Challenged Adipose Derived Stem Cells by Improving Autophagy

机译：雷帕霉素通过改善自噬作用促进缺血性脂肪衍生干细胞的存活和成脂

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>Background/Aims: Ischemia is one of the main causes of the high rate of absorption of transplanted autologous fat. Autophagy allows cells to survive by providing energy under starvation. Rapamycin has been found to play a role in promoting autophagy. In this study, we investigated whether rapamycin participates in the survival and adipogenesis of ischemia-challenged adipose-derived stem cells (ADSCs) by regulating autophagy. Methods: Before the cells were exposed to oxygen-glucose deprivation (OGD), a simulated ischemic microenvironment, the level of autophagy was reduced or increased by lentiviral transfection with short hairpin RNA targeting microtubule-associated protein 1-light chain 3 gene (shRNA-LC3) or treatment with rapamycin, respectively. The level of autophagy was assessed by western blotting, transmission electron microscopythen the apoptosis ratio was determined through terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) and flow cytometry. Adipogenesis was further evaluated by oil red O staining and the expressions level of some specific proteins for adipocytes. Results: shRNA-LC3 and rapamycin treatment effectively decreased and improved the level of autophagy in cells with or without OGD challenge, respectively. In addition, autophagy inhibition increased the apoptosis rate and activated caspase-3 expression level in response to OGD, and these were markedly inhibited by rapamycin preconditioning. During adipogenesis, autophagy inhibition decreased not only oil droplet accumulation but also lipoprotein lipase (LPL) and peroxisome proliferator-activated receptor gamma (PPAR?3) expression in cells with or without OGD challenge. However, autophagy promotion by rapamycin increased oil droplet accumulation and LPL and PPAR?3 expression. Conclusions: Rapamycin may promote the survival and adipogenesis of ischemia-challenged ADSCs by upregulating autophagy.
机译：> 背景/目的： 缺血是导致移植自体脂肪吸收率高的主要原因之一。自噬通过在饥饿状态下提供能量来使细胞存活。已经发现雷帕霉素在促进自噬中起作用。在这项研究中，我们研究了雷帕霉素是否通过调节自噬参与了缺血性挑战性脂肪干细胞（ADSCs）的存活和成脂。 方法： 在将细胞暴露于模拟的局部缺血微环境中的氧葡萄糖剥夺（OGD）之前，通过短发夹RNA慢病毒转染降低或增加自噬水平分别靶向微管相关蛋白1-轻链3基因（shRNA-LC3）或雷帕霉素治疗。通过蛋白质印迹法评估自噬水平，通过透射电镜观察，然后通过末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）和流式细胞术测定细胞凋亡率。通过油红O染色和一些特定的脂肪细胞蛋白表达水平进一步评估脂肪形成。 结果： shRNA-LC3和雷帕霉素处理分别有效降低和提高了OGD攻击或不存在OGD攻击的细胞的自噬水平。此外，自噬抑制作用增加了对OGD的凋亡率和激活的caspase-3表达水平，雷帕霉素预处理显着抑制了这些作用。在脂肪形成过程中，在有或没有OGD刺激的细胞中，自噬抑制作用不仅会降低油滴积累，而且会降低脂蛋白脂肪酶（LPL）和过氧化物酶体增殖物激活受体γ（PPAR？3）的表达。但是，雷帕霉素促进自噬会增加油滴的积累以及LPL和PPAR？3的表达。 结论： 雷帕霉素可能通过上调自噬来促进缺血性ADSC的存活和成脂。

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