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C-reactive protein induces p53-mediated cell cycle arrest in H9c2 cardiac myocytes

 Ji-Won Choi ; Kyung Hye Lee ; Ji Hyung Chung ; Seok-Min Kang ; Soo Young Kim ; Ho-Yeon Won ; Jaewon Oh ; Beom Seob Lee ; Taewon Jin ; Soo Hyuk Kim 
 Biochemical and Biophysicial Research Communications, Vol.410(3) : 525~530, 2011 
Journal Title
 Biochemical and Biophysicial Research Communications 
Issue Date
C-reactive protein (CRP) is one of the most important biomarker for cardiovascular diseases. Recent studies have shown that CRP affects cell survival, differentiation and apoptosis. However, the effect of CRP on the cell cycle has not been studied yet. We investigated the cell cycle alterations and cellular mechanisms induced by CRP in H9c2 cardiac myocytes. Flow cytometry analysis showed that CRP-treated H9c2 cells displayed cell cycle arrest in G0/G1 phase. CRP treatment resulted in a significant reduction in the levels of CDK4, CDK6 and cyclin D1 in a concentration-dependent manner. Interestingly, CRP caused an increase in the p53 accumulation and its phosphorylation on Ser15, leading to induce p21 upregulation. Treatment with a specific p53 inhibitor, PFT-α restored the levels of CDK4 and CDK6. A significant increase of ERK1/2 phosphorylation level was detected in CRP-treated cells. Furthermore, pretreatment of a specific ERK inhibitor resulted in decreased p53 phosphorylation and p21 induction. ERK inhibitor pretreatment induced significant restoration of protein levels of CDK4 and CDK6, leading to re-entry into the cell cycle. In addition, increased phosphorylation of p53 and ERK induced by CRP was considerably reversed by Fc gamma receptor IIIa (FcγRIIIa) knock-down using siRNA. FcγRIIIa siRNA transfection also restored the levels of cell cycle proteins. Our study has provided the first proposal on the novel insights into how CRP directly affects cell cycle in cells.
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Medical Research Center
1. 연구논문 > 5. Research Institutes > Cardiovascular Product Evaluation Center
1. 연구논문 > 1. College of Medicine > Dept. of Internal Medicine
1. 연구논문 > 1. College of Medicine > Yonsei Biomedical Research Center
Yonsei Authors
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