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

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 proliferati...

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Detalles Bibliográficos
Autores principales: Zhang, Danhuan, Xi, Minhui, Chen, Lingyun, Huang, Yanping, Mao, Peiju
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5774436/
https://www.ncbi.nlm.nih.gov/pubmed/29434706
http://dx.doi.org/10.3892/etm.2017.5521
Descripción
Sumario: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.