tRF-011690对阿霉素诱导的足细胞自噬的影响
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南京医科大学第二附属医院儿肾科

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江苏省自然科学基金(BK20211385)


Effects of tRF-011690 on podocyte autophagy induced by Adriamycin
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    摘要:

    目的:探究tRNA衍生片段-011690(tRNA-derived fragment-011690,tRF-011690)在阿霉素(Adriamycin, ADR)诱导的足细胞自噬中的作用及机制。方法:(1)用ADR(1 μg/mL)和tRF-011690 mimic干预足细胞,分为Control组、ADR组、ADR+tRF-011690 mimic组和ADR+tRF-011690 NC组。用RT-qPCR法检测各组tRF-011690、LC3Ⅱ/Ⅰ和p62的mRNA表达水平;Western blot法测定各组LC3Ⅱ/Ⅰ和p62蛋白的表达量。(2)用ADR和雷帕霉素(Rapamycin,200 ng/mL)干预足细胞,分为Control组、ADR组、ADR+Rapamycin组和Rapamycin组。用Western blot法检测各组p-mTOR、LC3Ⅱ/Ⅰ和p62蛋白相对表达,RT-qPCR法用来检测各组tRF-011690表达水平。结果:(1)同Control组相比,ADR组足细胞中tRF-011690表达水平下降,LC3Ⅱ/Ⅰ和p62表达量在蛋白和mRNA水平显著增加(P<0.05)。同ADR+NC组相比,ADR+tRF-011690 mimic组tRF-011690表达水平显著上升(P<0.05),证明tRF-011690过表达成功,LC3Ⅱ/Ⅰ和p62表达量在蛋白和mRNA水平显著下降低P<0.05)。(2)同Control组比,ADR组p-mTOR蛋白表达量增加,LC3Ⅱ/Ⅰ和p62蛋白相对表达降低,tRF-011690表达水平下降(P<0.05);同ADR组相比,ADR+Rapamycin组p-mTOR蛋白表达量降低,LC3Ⅱ/Ⅰ和 p62蛋白相对表达降低,tRF-011690表达显著上升(P<0.05)。结论:tRF-011690可能作为mTOR通路的下游效应分子抑制ADR诱导的足细胞自噬,为治疗慢性肾脏病提供了新的思路。

    Abstract:

    Objective: To explore the role and mechanism of tRNA-derived fragment-011690(tRF-011690)) in Adriamycin induced podocyte autophagy. Methods: (1) Podocytes were intervened with ADR (1 μg/mL) and tRF-011690 mimic, and were divided into Control group, ADR group, ADR+tRF-011690 mimic group and ADR+tRF-011690 NC group. The mRNA expression levels of tRF-011690, LC3II/Ⅰ and p62 were detected by RT-qPCR; Western blot was used to determine the expression of LC3II/Ⅰ and p62 protein. (2) Podocytes were intervened with ADR (1 μg/mL) and Rapamycin and divided into Control group, ADR group,ADR+Rapamycin group and Rapamycin group. The relative expression of p-mTOR, LC3II/Ⅰ and p62 proteins was detected by Western blot, and RT-qPCR was used to detect the expression level of tRF-011690. Results:(1) Compared with Control group, the expression level of tRF-011690 was decreased in ADR group, and the expression of LC3II/Ⅰ and p62 was significantly increased at protein and mRNA levels (P<0.05). Compared with ADR+NC group, tRF-011690 expression level in ADR+tRF-011690 mimic group increased significantly (P<0.05), which confirmed the tRF-011690 was successfully overexpressed, and LC3 II/Ⅰ and p62 expression decreased significantly under protein and mRNA levels P<0.05). (2) Compared with Control group, p-mTOR protein expression was increased in ADR group, relative expression of LC3 II/Ⅰ and p62 protein was decreased, and tRF-011690 expression level was decreased (P<0.05); compared with ADR group, p-mTOR protein expression was decreased in ADR+Rapamycin group, relative expression of LC3 II/Ⅰ and p62 protein was decreased and tRF-011690 expression significantly increased (P<0.05). Conclusion: tRF-011690 may act as a downstream effector molecule of the mTOR pathway, which provides a new approach for the treatment of chronic kidney disease.

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  • 收稿日期:2023-07-18
  • 最后修改日期:2023-07-18
  • 录用日期:2023-10-27
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