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- W3177178381 abstract "Kallikrein-related peptidase 8 (KLK8), a member of the tissue KLK family, has been identified in various tissues. The roles of KLK8 in cardiac pathologies remain unknown. In the present study, we found that KLK8 expression was upregulated in both hypertrophic hearts and hearts subjected to ischemia-reperfusion injury. KLK8 overexpression attenuated whereas KLK8 knockdown exacerbated hypoxia/reoxygenation-induced injury in primary cardiomyocytes of neonatal rat. The protective effects of KLK8 were abolished by kinin B2 receptor antagonist and in kinin B2 knockdown cells. Knockdown of KLK8 attenuated phenylephrine-induced cardiomyocyte hypertrophy. Overexpression of KLK8 induced cardiomyocyte hypertrophy, which was reversed by serine protease inhibitors, but not by kinin receptor antagonists. KLK8 overexpression resulted in a significant increase in epidermal growth factor (EGF) level in the culture media, which was abolished by serine protease inhibitors. EGF receptor antagonist AG1478 and siRNA targeting EGF receptor blocked the hypertrophic effects of KLK8 in cardiomyocytes. In conclusion, KLK8 initiates anti-apoptotic effect cardiomycytes via kinin B2 receptor, whereas it induces hypertrophy through EGF/EGFR signaling. This work is supported by NSFC (No. 31000516) and Science and Technology Commission of Shanghai Municipals (09XD1405600)." @default.
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- W3177178381 date "2013-04-01" @default.
- W3177178381 modified "2023-10-16" @default.
- W3177178381 title "Functional characterization of KLK 8 in cardiomyocytes: cardioprotection and induction of hypertrophy" @default.
- W3177178381 doi "https://doi.org/10.1096/fasebj.27.1_supplement.1188.6" @default.
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