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Kim, J. et al.

Jaetaek Kim, Ji-Hyun Ahn, Jeong-Hun Kim, Young-Suk Yu, Ho-Shik Kim, Joohun Ha, Soon-Hyun Shinn, Yeon-Sahng Oh,

Fenofibrate regulates retinal endothelial cell survival through the AMPK signal transduction pathway.

Fenofibrate, a widely used hypolipidemic drug, has anti-inflammatory and anti-atherosclerotic effects in the vessel wall. In the present study, we report an anti-apoptotic property of fenofibrate in human retinal endothelial cells (HRECs) and describe an underlying molecular mechanism. Treatment with fenofibrate protected HRECs from apoptosis in response to serum deprivation in a dose-dependent manner. This inhibition of apoptosis by fenofibrate was not altered by peroxisome proliferator-activated receptor alpha (PPARalpha) antagonist MK 886, and selective agonist for PPARalpha, WY-14643 had no beneficial effects on serum deprivation-induced cell death. Fenofibrate potently induced a sustained activation of AMP-activated protein kinase (AMPK) and vascular endothelial growth factor (VEGF) mRNA expression. Furthermore, compound C, a specific AMPK inhibitor, almost completely blocked the fenofibrate-induced survival effect as well as VEGF mRNA expression. Taken together, these results suggest that fenofibrate prevents apoptotic cell death induced by serum deprivation through PPARalpha-independent, but AMPK-dependent pathway. Thus fenofibrate may have a novel therapeutic property that can control unwanted cell death found in diabetic retinopathy.[1]

References

Fenofibrate regulates retinal endothelial cell survival through the AMPK signal transduction pathway. Kim, J., Ahn, J.H., Kim, J.H., Yu, Y.S., Kim, H.S., Ha, J., Shinn, S.H., Oh, Y.S. Exp. Eye Res. (2007) [Pubmed]

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