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PTX3 in serum induces renal mesangial cell proliferation but has no effect on apoptosis

机译:血清中的PTX3诱导肾小球膜细胞增殖但对细胞凋亡没有影响

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摘要

The present study aimed to investigate the effect of pentraxin 3 (PTX3) on the regulation of proliferation and apoptosis in human glomerular mesangial cells (HMCs). Small interfering (si)RNA was designed and synthesized to inhibit the expression of endogenous PTX3, and the effects on the proliferation and apoptosis of HMCs were detected by flow cytometry and an MTT assay. Western blot analysis was used to detect the activation of mitogen-activated protein kinase (MAPK) proteins in HMCs with PTX3 knockdown. Three siRNAs targeting PTX3 were individually transfected into HMCs for 48 h, and reverse-transcription quantitative PCR demonstrated that the relative mRNA expression of PTX3 was significantly decreased in all groups by up to 79.62% of that in the control group (P<0.05). Following transfection with PTX3-siRNA, the viability of an HMC line was significantly decreased in comparison with that of a control group transfected with scrambled siRNA. However, PTX3-siRNA did not significantly effect early and late apoptotic cell populations in HMCs compared with those in the control. Endogenous PTX3 interference was found to significantly decrease p38 MAPK, extracellular signal-regulated kinase 1/2 and c-Jun N-terminal kinase phosphorylation. In conclusion, silencing of PTX3, inhibited the proliferation of HMCs via MAPK pathways, but exerted no effect on the apoptosis of HMCs.
机译:本研究旨在探讨五味子蛋白3(PTX3)对人肾小球系膜细胞(HMCs)增殖和凋亡的调节作用。设计并合成了小干扰RNA(si),以抑制内源性PTX3的表达,并通过流式细胞术和MTT法检测了对HMC增殖和凋亡的影响。 Western blot分析用于检测具有PTX3抑制作用的HMC中丝裂原激活的蛋白激酶(MAPK)蛋白的激活。将三个靶向PTX3的siRNA分别转染到HMC中48 h,逆转录定量PCR结果显示,所有组中PTX3的相对mRNA表达均显着降低,最高达到对照组的79.62%(P <0.05)。用PTX3-siRNA转染后,HMC系的存活率与用杂乱siRNA转染的对照组相比明显降低。但是,与对照组相比,PTX3-siRNA不会显着影响HMC中的早期和晚期凋亡细胞群。发现内源性PTX3干扰可显着降低p38 MAPK,细胞外信号调节激酶1/2和c-Jun N端激酶磷酸化。总之,PTX3沉默可通过MAPK途径抑制HMC的增殖,但对HMC的凋亡没有影响。

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