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Regulator of G-protein signalling 5 deficiency impairs ventricular remodelling after myocardial infarction by promoting NF-κB and MAPK signalling in mice

Ding, Hua-Sheng, Huang, Yan, Chen, Zhen, Tang, Yan-Hong, Wang, Dan-Dan, Fan, Di, Huang, Cong-xin
Biochemical and biophysical research communications 2018 v.499 no.2 pp. 143-149
G-proteins, apoptosis, coronary vessels, heart, infarction, inflammation, knockout mutants, mice, mitogen-activated protein kinase, models, myocardial infarction, signal transduction, survival rate, transcription factor NF-kappa B
Regulator of G-protein signalling 5 (RGS5) is, highly expressed in different cell types of the adult human heart, and it is a negative regulator of G protein-mediated signalling that inactivates Gα(q) and Gα(i) and thereby inhibits many signalling pathways. However, the critical role of RGS5 in the pathology of myocardial infarction (MI) remains unexplored. Here, an in vitro MI model, induced by the permanent ligation of the left anterior descending coronary artery, was used with the isolated hearts of wild type (WT) and RGS5-knockout (KO) mice. Our results showed that the loss of RGS5 decreased the post-MI survival rate and left ventricular (LV) function and increased the infarct size. Additionally, the RGS5 knockout mice exhibited greater inflammation, apoptosis, and ventricular remodelling compared with WT-MI mice. Mechanistically, RGS5 loss activated the pathological response mainly by affecting the NF-κB and MAPK signalling pathways. Therefore, our data strongly indicate that RGS5 is a novel modulator of pathological progression after MI that functions NF-κB and MAPK signalling.