Yanyan Li, Zugui Huang, Chaoqun You, Qiao Chen, Dezhi Kong, Qifeng Wei, Bin Deng, Ting Chen, Zhanlin Liao, Liangzhi Huang
{"title":"糖尿病肾病中甲基 CpG 结合蛋白 2 的降调分析","authors":"Yanyan Li, Zugui Huang, Chaoqun You, Qiao Chen, Dezhi Kong, Qifeng Wei, Bin Deng, Ting Chen, Zhanlin Liao, Liangzhi Huang","doi":"10.1166/jbn.2024.3811","DOIUrl":null,"url":null,"abstract":"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\n 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\n 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\n 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,\n 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\n 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.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9000,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Down-Regulation Assession of Methyl CpG Binding Protein 2 in Diabetic Nephropathy\",\"authors\":\"Yanyan Li, Zugui Huang, Chaoqun You, Qiao Chen, Dezhi Kong, Qifeng Wei, Bin Deng, Ting Chen, Zhanlin Liao, Liangzhi Huang\",\"doi\":\"10.1166/jbn.2024.3811\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"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\\n 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\\n 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\\n 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,\\n 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\\n 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.\",\"PeriodicalId\":15260,\"journal\":{\"name\":\"Journal of biomedical nanotechnology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.9000,\"publicationDate\":\"2024-04-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of biomedical nanotechnology\",\"FirstCategoryId\":\"5\",\"ListUrlMain\":\"https://doi.org/10.1166/jbn.2024.3811\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of biomedical nanotechnology","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1166/jbn.2024.3811","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"Medicine","Score":null,"Total":0}
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.