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首页> 外文期刊>Cell biology international. >LINC00462 is involved in high glucose‐induced apoptosis of renal tubular epithelial cells via AKT pathway
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LINC00462 is involved in high glucose‐induced apoptosis of renal tubular epithelial cells via AKT pathway

机译：LINC00462通过AKT途径参与高葡萄糖诱导的肾小管上皮细胞凋亡

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Abstract New evidences suggest that long non‐coding RNAs (lncRNAs) may play important roles in a variety of kidney diseases, including diabetic nephropathy (DN). Our present study investigated the potential function of LINC00462 in high glucose (HG)‐induced apoptosis of renal tubular epithelial cells (RTEC) and to determine the underlying mechanism. The expression of LINC00462 in renal biopsy tissues was examined using quantitative reverse‐transcription polymerase chain reaction (qRT‐PCR). Then, a loss of function assay was performed to determine the protective effect of LINC00462 in HG‐induced RTEC damage. In addition, the downstream signaling pathway of LINC00462 was also investigated. The qRT‐PCR results showed that the expression of LINC00462 was significantly up‐regulated in renal biopsies from DN patients. At the same time, LINC00462 was enhanced in a glucose concentration‐ and time‐dependent manner in human kidney (HK‐2 and HKC) cells subjected to HG treatment. The knockdown of LINC00462 improved the significantly reduced cell viability of HG treatment, decreased HG‐induced reactive oxygen species (ROS) and malondialdehyde levels, and up‐regulated the response of antioxidant systems to ROS by increasing superoxide dismutase and catalase levels. In addition, knockdown of LINC00462 inhibited HG‐induced cell apoptosis and affected the expression of apoptosis‐related proteins. Most importantly, we found that knockdown of LINC00462 enhanced the expression of p‐AKT. Moreover, AKT‐specific inhibitor LY294002 restored the effect of LINC00462 knockdown on apoptosis. In conclusion, our study demonstrated that knockdown of LINC00462 can ameliorate oxidative stress and apoptosis in HG‐induced RTEC by activating the AKT pathway, suggesting that knockdown of LINC00462 may provide a potential therapeutic approach for DN.
机译：摘要新证据表明，长非编码RNA（lncRNAs）可能在包括糖尿病肾病（DN）在内的多种肾脏疾病中发挥重要作用。我们目前的研究调查了LINC00462在高糖（HG）诱导的肾小管上皮细胞（RTEC）凋亡中的潜在功能，并确定其潜在机制。使用定量逆转录聚合酶链反应（qRT-PCR）检测肾活检组织中LINC00462的表达。然后，进行功能丧失试验，以确定LINC00462在汞诱导的RTEC损伤中的保护作用。此外，还研究了LINC00462的下游信号通路。qRT-PCR结果显示，在DN患者的肾活检中，LINC00462的表达显著上调。同时，在接受汞处理的人类肾脏（HK-2和HKC）细胞中，LINC00462以葡萄糖浓度和时间依赖性的方式增强。LINC00462的敲除改善了汞处理显著降低的细胞活力，降低了汞诱导的活性氧（ROS）和丙二醛水平，并通过增加超氧化物歧化酶和过氧化氢酶水平来上调抗氧化系统对ROS的反应。此外，敲除LINC00462可抑制汞诱导的细胞凋亡，并影响凋亡相关蛋白的表达。最重要的是，我们发现敲除LINC00462可增强p-AKT的表达。此外，AKT特异性抑制剂LY294002恢复了LINC00462基因敲除对细胞凋亡的影响。总之，我们的研究表明，敲除LINC00462可以通过激活AKT途径改善汞诱导的RTEC中的氧化应激和凋亡，这表明敲除LINC00462可能为DN提供了一种潜在的治疗方法。

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