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Anti-inflammatory effect of PPARgamma in cultured human mesangial cells
Zuying Xiong1, Haichang Huang, Jingzi Li
1Renal Division of First Hospital and Institute of Nephrology, Peking University, Beijing, China.
Abstract:
Our aim is to investigate whether peroxisome proliferator-activator receptor-gamma (PPARgamma) expression was altered in human mesangial cells under inflammatory stress and whether PPARgamma could retard the inflammatory responses. Based on cultured human mesangial cell lines (HMCLs), PPARgamma expressions at protein and mRNA levels were observed by Western blot analysis and reverse transcriptase polymerase chain reaction. Informatory cytokines such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) were measured by enzyme-linked immunosorbent assay. Our results demonstrated that PPARgamma protein expression was dramatically increased in HMCLs stimulated by IL-1beta (10 ng/mL). The levels of IL-6 and TNF-alpha in HMCL supernatants, protein, and mRNA expressions of PPARgamma in IL-1beta challenge cells were significantly increased more than those in untreated cells. Importantly, PPARgamma agonists troglitazone, rosiglitazone, and 15-deoxy-delta(12, 14)-prosglandin J2 significantly decreased the up expression of TNF-alpha and IL-6 in HMCL supernatants stimulated by IL-1beta. Furthermore, troglitazone downregulated TNF-alpha and IL-6 mRNA expression from IL-1beta challenge HMCLs. Our data suggest that PPARgamma plays an important role in mesangial cells responding to inflammatory stress. PPARgamma may prove to be a pharmacological target in glomerulonephritis.
Insights
Peroxisome proliferator-activator receptor-gamma (PPARgamma) increases with inflammatory stress in human mesangial cells. PPARgamma agonists reduce inflammatory responses, suggesting its potential as a therapeutic target for glomerulonephritis.
Area of Science:
- Nephrology
- Molecular Biology
- Immunology
Background:
- Inflammatory stress significantly impacts kidney function.
- Mesangial cells play a crucial role in glomerular inflammation.
- The role of PPARgamma in mesangial cell inflammatory responses requires elucidation.
Purpose of the Study:
- To investigate PPARgamma expression in human mesangial cells under inflammatory conditions.
- To determine if PPARgamma can mitigate inflammatory responses in these cells.
- To explore PPARgamma as a potential therapeutic target for glomerulonephritis.
Main Methods:
- Cultured human mesangial cell lines (HMCLs) were utilized.
- PPARgamma protein and mRNA levels were assessed via Western blot and RT-PCR.
- Inflammatory cytokines (TNF-alpha, IL-6) were quantified using ELISA.
Main Results:
- IL-1beta stimulation significantly increased PPARgamma protein and mRNA expression in HMCLs.
- Elevated levels of TNF-alpha and IL-6 were observed in stimulated HMCLs.
- PPARgamma agonists (troglitazone, rosiglitazone, 15-d-PGJ2) effectively reduced TNF-alpha and IL-6 expression.
Conclusions:
- PPARgamma expression is upregulated in mesangial cells during inflammatory stress.
- PPARgamma activation demonstrates anti-inflammatory effects in mesangial cells.
- Targeting PPARgamma may offer a novel therapeutic strategy for inflammatory kidney diseases like glomerulonephritis.
