1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) Induces Cell Apoptosis of Human Mesangial Cells

IF 0.1 4区 生物学 Q4 GENETICS & HEREDITY International Journal of Human Genetics Pub Date : 2022-09-01 DOI:10.31901/24566330.2022/22.03.821
Chunjian Zhang
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Abstract

In China, primary glomerulonephritis is the leading cause of end-stage renal disease (ESRD), and patients who require kidney transplantation often with ESRD. Glomerulonephritis primary’s most prevalent subtype is Mesangial proliferative glomerulonephritis (MsPGN). Although the cell apoptosis of human mesangial cells (HMCs) may be harmful in MsPGN, it plays a major role in the elimination of excessive HMCs and reparative glomerular remodelling after inflammation. A powerful mitogen for growing mesangial cells is epidermal growth factor (EGF). Therefore, it is possible to induce the proliferation of HMCs by incubating with EGF in vitro. 1,25(OH)2D3(VD3) may cause cell death in HMCs via activating AKT, caspase-3, caspase-9, JNK, and ERK, as well as elevating Bax and Bad levels.
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1,25-二羟基维生素D3(1,25-(OH)2D3)诱导人系膜细胞凋亡
在中国,原发性肾小球肾炎是终末期肾病(ESRD)的主要原因,需要肾移植的患者往往伴有ESRD。原发性肾小球肾炎最常见的亚型是系膜增生性肾小球肾炎(MsPGN)。虽然人系膜细胞(HMCs)的细胞凋亡在MsPGN中可能是有害的,但它在消除过量的HMCs和炎症后的修复性肾小球重塑中起着重要作用。一个强大的分裂原生长系膜细胞是表皮生长因子(EGF)。因此,体外培养EGF诱导hmc增殖是可能的。1,25(OH)2D3(VD3)可能通过激活AKT、caspase-3、caspase-9、JNK和ERK,以及升高Bax和Bad水平而导致hmc细胞死亡。
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