糖尿病肾病中甲基 CpG 结合蛋白 2 的降调分析

IF 2.9 4区 医学 Q1 Medicine
Yanyan Li, Zugui Huang, Chaoqun You, Qiao Chen, Dezhi Kong, Qifeng Wei, Bin Deng, Ting Chen, Zhanlin Liao, Liangzhi Huang
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引用次数: 0

摘要

糖尿病肾病(DN)是全球糖尿病最重要的微血管并发症,是由高血糖诱导的荚膜细胞损伤和凋亡引起的。人们已经观察到甲基 CpG 结合蛋白 2(MECP2)的作用,但其在 DN 中的具体参与情况仍不清楚。本研究利用暴露于高葡萄糖(HG,30 mM)的人肾小球荚膜细胞建立了体外 DN 模型。使用 qRT-PCR 和 Western Blot 评估了 MECP2 的表达。在 HG 组和 HG + MECP2 敲除组中,通过 CCK-8 和 transwell 试验评估增殖和迁移。细胞凋亡通过流式细胞术和 Western 印迹进行评估。RNA测序确定了HG组和HG+MECP2敲除组之间的差异表达基因(DEGs),随后利用KEGG和GSEA数据库进行了富集分析。我们的结果表明,与对照组相比,HG 处理的荚膜细胞中 MECP2 表达升高。与 HG 组相比,敲除 MECP2 的荚膜细胞增殖和迁移能力增强。在 HG+MECP2 shRNA 组中,促凋亡蛋白(cleaved-caspase3、Bax、BAD、Desmin)的表达较低,而抗凋亡蛋白 Bcl-2 的表达较高。RNA 测序确定了 123 个上调的 DEGs 和 129 个下调的 DEGs。富集分析强调了与凋亡相关的通路,如 PPAR、TNF、p53、RELAXIN、WNT 和 RAP1 信号转导。敲除 MECP2 的荚膜细胞在 HG 处理后凋亡减少。总之,下调荚膜细胞中的 MECP2 能有效减轻高血糖引起的细胞凋亡,是改善糖尿病肾病预后的一种潜在策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Down-Regulation Assession of Methyl CpG Binding Protein 2 in Diabetic Nephropathy
Diabetes nephropathy (DN) is the most significant microvascular complication of diabetes worldwide due to hyperglycemiainduced podocyte injury and apoptosis. The role of methyl CpG binding protein 2 (MECP2) has been observed, but its specific involvement in DN remains unclear. In this study, an in vitro DN model was established using human glomerular podocytes exposed to high glucose (HG, 30 mM). MECP2 expression was assessed using qRT-PCR and Western Blot. Proliferation and migration were evaluated through CCK-8 and transwell assays in both the HG group and the HG + MECP2 knockdown group. Apoptosis was assessed by flow cytometry and Western Blot. RNA-Sequencing identified differentially expressed genes (DEGs) between HG and HG+MECP2 knockdown groups, with subsequent enrichment analysis using KEGG and GSEA databases. Our results revealed elevated MECP2 expression in HG-treated podocytes compared to the control group. Podocytes with MECP2 knockdown displayed increased proliferation and migration compared to the HG group. MECP2 knockdown significantly inhibited HG-induced apoptosis in podocytes, with lower expression of pro-apoptotic protein (cleaved-caspase3, Bax, BAD, Desmin) and higher expression of anti-apoptotic protein Bcl-2 in the HG+MECP2 shRNA group. RNA sequencing identified 123 upregulated and 129 downregulated DEGs. Enrichment analysis highlighted apoptosis-related pathways like PPAR, TNF, p53, RELAXIN, WNT, and RAP1 signaling. Podocytes with MECP2 knockdown showed reduced apoptosis upon HG treatment. In summary, downregulation of MECP2 in podocytes effectively mitigated apoptosis caused by high glucose, suggesting a potential strategy to improve diabetes nephropathy outcomes.
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来源期刊
CiteScore
4.30
自引率
17.20%
发文量
145
审稿时长
2.3 months
期刊介绍: Information not localized
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