Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8644634 | Gene | 2018 | 15 Pages |
Abstract
Farnesyl pyrophosphate synthase (FPPS) is a vital enzyme in the mevalonate pathway. Our previous study has indicated that overexpression of FPPS increases hypoxia/reoxygenation (HR) injury in Heart-derived H9c2 Cells. Hence, we designed this experiment to further investigate the effect of FPPS on myocardial ischemia/reperfusion (MIR) injury using a transgenic (Tg) model, and explore the relevant mechanisms. The results showed that when mouse hearts were subjected to ex vivo I/R, Tg mice have a higher CK and LDH, a larger myocardial infarct size and lower heart function recovery. These phenomena are associated with the increased Rac1 activity and ROS generation. These findings point to that FPPS might be a potential target in preventing MIR in vivo.
Keywords
MIRLangendorffFPPSGGPPRac1ATCCHRPFPPPVDFDMEMFBSDulbecco's modified Eagle MediumROSSDS-PAGEMyocardial ischemia/reperfusionpolyvinylidene difluoridefetal bovine serumShrfarnesyl pyrophosphate synthaselactate dehydrogenaseLDHAmerican Type Culture CollectionSpontaneously hypertensive ratsHorseradish peroxidasegeranylgeranyl pyrophosphateCreatine kinaseReactive oxygen species
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Authors
Dongpu Dai, Xiaotong Sun, Jie Ding, Yuxiao Chen, Shenjiang Hu,