scholarly journals The C-Terminal Module IV of Connective Tissue Growth Factor, Through EGFR/Nox1 Signaling, Activates the NF-κB Pathway and Proinflammatory Factors in Vascular Smooth Muscle Cells

2015 ◽  
Vol 22 (1) ◽  
pp. 29-47 ◽  
Author(s):  
Raúl R. Rodrigues-Diez ◽  
Ana Belen Garcia-Redondo ◽  
Macarena Orejudo ◽  
Raquel Rodrigues-Diez ◽  
Ana Maria Briones ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Connective Tissue ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Connective Tissue Growth Factor ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Tissue Growth ◽  
Proinflammatory Factors

scholarly journals Magnolol, A Novel Antagonist of Thrombin and PAR-1, Inhibits Thrombin-Induced Connective Tissue Growth Factor (CTGF) Expression in Vascular Smooth Muscle Cells and Ameliorate Pathogenesis of Restenosis in Rats

2020 ◽  
Vol 10 (23) ◽  
pp. 8729
Author(s):  
Wen-Chin Ko ◽  
Chia-Ti Tsai ◽  
Kai-Cheng Hsu ◽  
Yu-Che Cheng ◽  
Tony Eight Lin ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Connective Tissue ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Connective Tissue Growth Factor ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Tissue Growth ◽  
Functional Assay

Restenosis and destructive vascular remodeling are the main reasons for treatment failure in patients undergoing percutaneous coronary intervention (PCI). In this study, we explored the efficacy of magnolol (a traditional Chinese medicine) in the treatment of restenosis. The results of this study showed that the activities of thrombin and PAR-1 (protease-activated receptor 1) were significantly decreased by the treatment of magnolol. Based on protein docking analysis, magnolol exhibits its potential to bind to the PAR-1 active site. In addition, thrombin-induced connective tissue growth factor (CTGF) expression and the upstream of CTGF such as JNK-1 (but not JNK-2), c-Jun, and AP-1 were distinctly inhibited by magnolol (50 μM) in vascular smooth muscle cells (VSMC). For the functional assay, magnolol (50 μM) significantly inhibited the migration of VSMC, and rats treated with magnolol (13 mg/kg/day) after balloon angioplasty has observed a significant reduction in the formation of common arterial neointima. In conclusion, we identified a novel mechanism by which magnolol acts as the thrombin activity inhibitor and may be the PAR-1 antagonist. In accordance with these functions, magnolol could decrease thrombin-induced CTGF expression in VSMCs via PAR-1/JNK-1/AP-1 signaling.

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