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Overexpression of SP1 restores autophagy to alleviate acute renal injury induced by ischemia-reperfusion through the miR-205/PTEN/Akt pathway
Journal of Inflammation ( IF 5.1 ) Pub Date : 2021-02-05 , DOI: 10.1186/s12950-021-00270-y
Chong Huang , Yan Chen , Bin Lai , Yan-Xia Chen , Cheng-Yun Xu , Yuan-Fei Liu

Acute kidney injury (AKI) is a major kidney disease with poor clinical outcome. SP1, a well-known transcription factor, plays a critical role in AKI and subsequent kidney repair through the regulation of various cell biologic processes. However, the underlying mechanism of SP1 in these pathological processes remain largely unknown. An in vitro HK-2 cells with anoxia-reoxygenation injury model (In vitro simulated ischemic injury disease) and an in vivo rat renal ischemia-reperfusion injury model were used in this study. The expression levels of SP1, miR-205 and PTEN were detected by RT-qPCR, and the protein expression levels of SP1, p62, PTEN, AKT, p-AKT, LC3II, LC3I and Beclin-1 were assayed by western blot. Cell proliferation was assessed by MTT assay, and the cell apoptosis was detected by flow cytometry. The secretions of IL-6 and TNF-α were detected by ELISA. The targeted relationship between miR-205 and PTEN was confirmed by dual luciferase report assay. The expression and positioning of LC-3 were observed by immunofluorescence staining. TUNEL staining was used to detect cell apoptosis and immunohistochemical analysis was used to evaluate the expression of SP1 in renal tissue after ischemia-reperfusion injury in rats. The expression of PTEN was upregulated while SP1 and miR-205 were downregulated in renal ischemia-reperfusion injury. Overexpression of SP1 protected renal tubule cell against injury induced by ischemia-reperfusion via miR-205/PTEN/Akt pathway mediated autophagy. Overexpression of SP1 attenuated renal ischemia-reperfusion injury in rats. SP1 overexpression restored autophagy to alleviate acute renal injury induced by ischemia-reperfusion through the miR-205/PTEN/Akt pathway.

中文翻译:

SP1的过表达恢复自噬,以缓解通过miR-205 / PTEN / Akt通路引起的缺血再灌注引起的急性肾损伤

急性肾损伤(AKI)是一种主要的肾脏疾病,临床预后较差。SP1是一种众所周知的转录因子,它通过调节各种细胞生物学过程在AKI和随后的肾脏修复中起关键作用。但是,在这些病理过程中,SP1的潜在机制仍然未知。本研究使用了具有缺氧-再氧化损伤模型(体外模拟缺血性损伤疾病)的体外HK-2细胞和体内大鼠肾缺血-再灌注损伤模型。通过RT-qPCR检测SP1,miR-205和PTEN的表达水平,并通过蛋白质印迹法检测SP1,p62,PTEN,AKT,p-AKT,LC3II,LC3I和Beclin-1的蛋白表达水平。通过MTT分析评估细胞增殖,并通过流式细胞术检测细胞凋亡。通过ELISA检测IL-6和TNF-α的分泌。通过双重荧光素酶报告测定证实了miR-205和PTEN之间的靶向关系。通过免疫荧光染色观察LC-3的表达和定位。TUNEL染色检测细胞凋亡,免疫组织化学分析评价大鼠缺血再灌注后肾组织SP1的表达。肾缺血再灌注损伤中PTEN的表达上调,而SP1和miR-205的表达下调。SP1的过表达保护肾小管细胞免受通过miR-205 / PTEN / Akt途径介导的自噬引起的缺血再灌注损伤。SP1的过表达减轻了大鼠的肾脏缺血再灌注损伤。
更新日期:2021-02-05
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