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首页> 外文期刊>Journal of cellular physiology. >Lin28a protects against diabetic cardiomyopathy through Mstl inhibition
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Lin28a protects against diabetic cardiomyopathy through Mstl inhibition

机译：Lin28a预防糖尿病心肌病通过Mstl抑制

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摘要

Lin28a has been found to enhance glucose uptake and insulin sensitivity. Lin28a alleviates cardiac dysfunction under various pathological conditions. However, the effects and underlying mechanisms of Lin28a on diabetic cardiomyopathy (DCM) are not well-understood. The aim of this study was to determine whether Lin28a protects against DCM and the potential mechanisms. Two to three days old mouse neonatal primary cardiomyocytes were randomized for treatment with adenoviruses harboring Lin28a and mammalian sterile 20-like kinase 1 (Mstl) short hairpin RNA, 48 hr before culturing in normal or high glucose medium. Cardiomyocyte apoptosis, autophagy, mitochondrial morphology, adenosine triphosphate content, and cytokine levels in the high glucose or normal conditions were observed between all groups. Either Lin28a overexpression or Mstl knockdown alleviated mitochondrial ultrastructure impairment, decreased cytokine levels, inhibited apoptosis, and enhanced autophagy in primary neonatal mouse cardiomyocytes treated with high glucose. Importantly, the protective effects of Lin28a and Mstl disappeared after treatment with 3-methyladenine, an autophagy inhibitor. Interestingly, in Mstl knockdown cardiomyocytes, Lin28a overexpression failed to further enhance autophagy and alleviate high glucose-induced cardiomyocyte injury, which implies the protective roles of Lin28a counteracting high glucose-induced cardiomyocyte injury are dependent on Mstl inhibition. Furthermore, co-immunoprecipitation and immunofluorescence double staining suggested that there were no direct interactions between Mstl and Lin28a. Lin28a increased the expression of Akt, which inhibited the activation of Mst1-mediated apoptotic pathways.
机译：Lin28a已经发现提高葡萄糖吸收和胰岛素敏感性。心脏功能障碍在不同病理条件。Lin28a机制在糖尿病心肌病(DCM)不容易理解。研究旨在确定是否Lin28a保护对DCM和潜在机制。三天的老老鼠新生儿初选心肌细胞被随机分配接受治疗腺病毒窝藏Lin28a和哺乳动物无菌20-like激酶1 (Mstl)短发夹RNA, 48小时前培养在正常或高葡萄糖的媒介。自噬,线粒体形态、腺苷三磷酸腺苷含量和细胞因子水平高葡萄糖或正常情况下被观察到所有组之间。或Mstl击倒减轻线粒体超微结构损伤,降低细胞因子水平,抑制细胞凋亡,增强自噬在初级新生儿鼠标心肌细胞治疗高葡萄糖。重要的是,Lin28a的保护作用Mstl治疗后消失自噬抑制剂3-methyladenine。有趣的是,在Mstl击倒的心肌细胞,Lin28a过度未能进一步加强自噬和缓解高glucose-induced心肌细胞损伤,这意味着保护的角色Lin28a抵消高glucose-induced心肌细胞损伤是依赖Mstl抑制。co-immunoprecipitation和免疫荧光双染色建议没有直接Mstl和Lin28a之间的相互作用。Lin28a Akt的表达增加,抑制Mst1-mediated的激活凋亡通路。

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