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Updated: Feb 14, 2026

Optimizing Isolation and Purification of Murine Glomerular Mesangial Cells
Published on: March 7, 2025
PTX3 in serum induces renal mesangial cell proliferation but has no effect on apoptosis
Danhuan Zhang1, Minhui Xi2, Lingyun Chen1
1Department of Nephrology, Tongren Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai 200336, P.R. China.
Abstract:
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.
Insights
Silencing pentraxin 3 (PTX3) in human glomerular mesangial cells (HMCs) inhibits proliferation via MAPK pathways. This study found PTX3 knockdown reduced HMC viability but did not affect apoptosis.
Area of Science:
- Nephrology
- Cell Biology
- Molecular Biology
Background:
- Pentraxin 3 (PTX3) is a key component of the innate immune system.
- Its role in regulating human glomerular mesangial cell (HMC) proliferation and apoptosis requires further investigation.
Purpose of the Study:
- To investigate the effect of pentraxin 3 (PTX3) on the regulation of proliferation and apoptosis in human glomerular mesangial cells (HMCs).
Main Methods:
- Small interfering (si)RNA was used to inhibit endogenous PTX3 expression in HMCs.
- Cell proliferation was assessed using MTT assays, and apoptosis was analyzed by flow cytometry.
- Western blot analysis was performed to detect mitogen-activated protein kinase (MAPK) pathway activation.
Main Results:
- PTX3-siRNA significantly decreased PTX3 mRNA expression in HMCs.
- HMC viability was significantly reduced following PTX3 knockdown.
- PTX3 silencing led to decreased phosphorylation of p38 MAPK, ERK1/2, and JNK signaling pathways.
- No significant effect on early and late apoptotic cell populations was observed.
Conclusions:
- Silencing PTX3 inhibits HMC proliferation through the MAPK signaling pathways.
- PTX3 does not appear to influence HMC apoptosis.
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