Analysis of signaling of Hexokinase 2 and MAS receptor in the cardiomyopathy overexpressing a set of microRNA
Description: The transgenic mice that express miR-143/145 in the cardiomyocytes (miRTG) exhibit the cardiomyopathy, but down-regulation of hexokinase 2 would not be involved in the pathogenesis. In the hearts of these mice, GSH and the ratio of GSH/GSSG increases, suggesting the activation of pentose phosphate pathway. With aging, the expression of angiotensin converting enzyme (ACE), and the phosphorylation of insulin-like growth factor 1 receptor (IGF1R) increases. ACE inhibitor improves the survival rate of miRTG, and suppresses the phosphorylation of IGF1R. Since the transgenic mice overexpressing MAS receptor in the cardiomyocytes (MASTG)unexpectedly display the cardiomyopathy, we are not able to do crossbreeding experiments between miRTG and MASTG.Together, miRTG would be a novel model for analyzing the molecular mechanism of cardiomyopathy with reductive state.
Amount: ¥4,810,000
Funding type: research
Funder scheme: Grant-in-Aid for Scientific Research (C)
Start date: 2016-04-01
End date: 2019-03-31
Investigator: Takashi IWAMOTO
Institution: Chubu University
Funded outputs count: 3
Funder award ID: 16K08748
OpenAlex ID: G240818643