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-  2018 

P58~(IPK)基因在视网膜Müller细胞内质网应激PERK通道中的作用 Role of P58~(IPK) Gene in PERK Pathway of ERS in Retina Müller Cells

Keywords: P58IPK,视网膜Müller细胞,内质网应激

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Abstract:

目的:探讨P58~(IPK)在高糖诱导视网膜Müller细胞内质网应激(ERS)PERK通道中的作用。方法:体外培养Müller细胞株(rMC-1),建立高糖模型,构建/P58~(IPK)基因敲除P58~(IPK)基因过表达质粒并转染到Müller细胞中,采用RT-PCR检测上游分子PERK的mRNA的表达、Western Blot检测Müller细胞p-PERK蛋白的表达,分析存在的差异,初步探讨P58~(IPK)在高糖诱导视网膜Müller细胞内质网应激PERK通道中的作用。结果:(1)荧光定量PCR检测结果显示:(1)未转入质粒组、转染P58~(IPK)基因敲除质粒组、转染P58~(IPK)基因过表达质粒组三组的细胞在5和25mmol/L糖浓度下培养时,各组内PERK mRNA的相对表达量相比,差异没有统计学差异(P>0.05)。(2)未转入质粒组、转染P58~(IPK)基因敲除质粒组、转染P58~(IPK)基因过表达质粒组三组的细胞在5和25mmol/L糖浓度下培养时,各组之间PERK mRNA的相对表达量,差异无统计学意义(P>0.05)。(2)Western Blot检测结果显示:(1)未转入质粒组、转染P58~(IPK)基因敲除质粒组、转染P58~(IPK)基因过表达质粒组三组的细胞在5和25mmol/L糖浓度下培养时,各组内p-PERK蛋白的表达量相比,差异有统计学差异(P<0.05)。(2)未转入质粒组、转染P58~(IPK)基因敲除质粒组、转染P58~(IPK)基因过表达质粒组三组的细胞在5和25mmol/L糖浓度下培养时,各组之间p-PERK蛋白的表达量,差异有统计学差异(P<0.05)。结论:高浓度葡萄糖的刺激下,视网膜Müller细胞会出现内质网应激反应,P58~(IPK)可靶向结合PERK抑制通道激活,减少蛋白质的翻译和合成,减轻内质网的蛋白负荷,减少ERS对细胞的损伤

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