YC-1 induces heat shock protein 70 expression and prevents oxidized LDL-mediated apoptosis in vascular smooth muscle cells

Shock
Yi-Nan LiuChe-Ming Teng

Abstract

Heat shock protein 70 (hsp70) functioning as molecular chaperon in physiological conditions is induced under stress environment, which affords a defensive mechanism for cells to escape cellular damage. Hence, it is a critical issue to develop a nontoxic hsp70-inducing compound against cellular death. The present study was conducted to evaluate whether 3-(5'-hydroxymethyl-2'-furyl)-1-benzyl-indazol (YC-1) can effectively induce hsp70 expression and protect vascular smooth muscle cells (VSMCs) against oxidized low-density lipoprotein-induced cytotoxicity. We showed that YC-1 enhanced hsp70 expression in VSMCs through a concentration- and time-dependent manner with maximum expression at 18 and 24 h without involving the cyclic guanosine monophosphate and reactive oxygen species signal in the pathway. Furthermore, we did not observe significant cytotoxicity after YC-1 treatment through 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, lactic dehydrogenase, and fluorescence activating cell sorting scan assays. We demonstrated that the nuclear level of heat shock transcription factor 1 increased at 2 h after YC-1 treatment, and hsp70 expression was directed by the up-regulation of hsp70 mRNA, which peaked at 6 h and was f...Continue Reading

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Citations

Jun 27, 2009·Biochemical and Biophysical Research Communications·Rui ZhanLing-Jia Qian
Dec 12, 2012·European Journal of Pharmacology·Kwok-Keung LamMao-Hsiung Yen
Aug 19, 2008·Shock·Christoph Thiemermann
Feb 25, 2009·Expert Opinion on Therapeutic Targets·Agata Bielecka-DabrowaMaciej Banach

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Apoptosis

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