Glucose induces apoptosis of cardiomyocytes via microRNA-1 and IGF-1 |
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Authors: | Yu Xi-Yong Song Yao-Hua Geng Yong-Jian Lin Qiu-Xiong Shan Zhi-Xin Lin Shu-Guang Li Yangxin |
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Affiliation: | a Texas Heart Institute and University of Texas Health Science Center, Heart Failure and Stem Cell, 6770 Bertner Avenue, Houston, TX 77030, USA b Research Center of Medical Sciences, Guangdong Provincial People’s Hospital, Guangdong Provincial Cardiovascular Institute, Guangzhou, Guangdong 510080, PR China c Department of Molecular Pathology, University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA |
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Abstract: | Glucose toxicity is an important initiator of cardiovascular disease, contributing to the development of cardiomyocyte death and diabetic complications. The present study investigated whether high glucose state could induce apoptosis of rat cardiomyocyte cell line H9C2 through microRNA regulated insulin-like growth factor (IGF-1) signaling pathway. Our data showed that H9C2 cells exposed to high glucose have increased miR-1 expression level, decreased mitochondrial membrane potential, increased cytochrome-c release, and increased apoptosis. Glucose induced mitochondrial dysfunction, cytochrome-c release and apoptosis was blocked by IGF-1. Using prediction algorithms, we identified 3′-untranslated regions of IGF-1 gene are the target of miR-1. miR-1 mimics, but not mutant miR-1, blocked the capacity of IGF-1 to prevent glucose-induced mitochondrial dysfunction, cytochrome-c release and apoptosis. In conclusion, our data demonstrate that IGF-1 inhibits glucose-induced mitochondrial dysfunction, cytochrome-c release and apoptosis and IGF-1’s effect is regulated by miR-1. |
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Keywords: | Glucose IGF-1 microRNA Apoptosis Cytochrome-c Mitochondria |
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