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Updated: May 29, 2026
Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
Published on: August 3, 2018
Effect of simvastatin on expression of transforming growth factor-β and collagen type IV in rat mesangial cells
Yan-Bo Li1, Jia-Jing Yin, Hong-Jie Wang
1Department of Endocrinology, First Affiliated Hospital of Harbin Medical University, Harbin, China. liyanbohyd@hotmail.com
Objective:
Diabetic nephropathy is characterized by the accumulation of extracellular matrix in the glomerular mesangium as a result of an imbalance between matrix synthesis and degradation. Since simvastatin has been proposed to decrease renal interstitial fibrosis, we hypothesized that the protective effect of statins was related to the expression of transforming growth factor-β (TGF-β) and type IV collagen (Col IV).
Methods:
Cultured rat mesangial cells (RMC) were exposed to high glucose (HG), advanced glycosylation end products (AGE) or H(2)O(2) in the absence and presence of simvastatin. Expression of TGF-β and Col IV was determined by Western blotting.
Results:
Coincubation of RMC with HG, AGE or H(2)O(2) resulted in a significant increase of the expression of TGF-β and Col IV (p < 0.05). Simvastatin significantly inhibited HG-, AGE- or H(2)O(2)-induced expression of TGF-β and Col IV (p < 0.05). Moreover, simvastatin also inhibited HG-, AGE- and H(2)O(2)-induced activation of p38 mitogen-activated protein kinase, which indicated that the preventive effect of simvastatin on TGF-β and Col IV may be associated with p38.
Conclusion:
These findings suggest that simvastatin can reduce HG-, AGE- and H(2)O(2)-induced expression of TGF-β and Col IV by inhibition of the p38 pathway.
Insights
Simvastatin reduces the expression of transforming growth factor-β (TGF-β) and type IV collagen (Col IV) in rat mesangial cells. This protective effect against high glucose, AGEs, and H2O2 may involve the inhibition of the p38 pathway.
Area of Science:
- Nephrology
- Cell Biology
- Pharmacology
Background:
- Diabetic nephropathy involves extracellular matrix accumulation in glomeruli.
- Simvastatin is proposed to mitigate renal interstitial fibrosis.
Purpose of the Study:
- To investigate if simvastatin's protective effects in diabetic nephropathy are linked to transforming growth factor-β (TGF-β) and type IV collagen (Col IV) expression.
- To explore the role of the p38 mitogen-activated protein kinase pathway.
Main Methods:
- Rat mesangial cells (RMC) were treated with high glucose (HG), advanced glycosylation end products (AGE), or H2O2.
- Simvastatin was added in the presence and absence of these treatments.
- Western blotting was used to measure TGF-β and Col IV expression and p38 activation.
Main Results:
- HG, AGE, and H2O2 significantly increased TGF-β and Col IV expression in RMC.
- Simvastatin significantly inhibited this HG-, AGE-, and H2O2-induced expression.
- Simvastatin also inhibited the activation of p38 mitogen-activated protein kinase.
Conclusions:
- Simvastatin reduces the expression of TGF-β and Col IV induced by HG, AGE, and H2O2.
- The protective mechanism of simvastatin appears to involve the inhibition of the p38 pathway.
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