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PKC Mediates PACSIN2 to Regulate Hypertrophic Cardiomyocytes in the Aggravation of the Compensatory Function


 Background Myocardial hypertrophy (MH) is an independent risk factor for cardiovascular and cerebrovascular events in patients with hypertension and myocardial infarction. Recent studies have shown that PACSIN2 is associated with cardiovascular disease; however, the function of cardiomyocytes remains unclear. Here, the interaction between protein kinase C‎‎ (PKC) and PACSIN2 and the manner in which PACSIN2 regulates MH was studied. Methods The cell models were constructed with angiotensin II (AII) and PMA; qRT-PCR and Western Blot were used to verify the relative protein expression of PKC and PACSIN2; immunofluorescence was used to determine the effect of PKC upregulation on the morphology of hypertrophic cardiomyocytes after an overexpression and silencing of PACSIN2 by qRT-PCR and Western blot analysis. Results The results indicate that PKC positively regulates the expression of PACSIN2 and causes MH phenotype. The overexpression of PACSIN2 was not solely responsible for MH, while the overexpression of PACSIN2 under MH caused hypertrophy to increase. In addition, the high expression of PACSIN2 caused an increase in α-MHC mRNA, but it was not related to the expression of tubulin. The morphological results indicate that the overexpression of PKC causes MH, which causes heart failure. Conclusion Studies have shown that PACSIN2 plays an important role in maintaining myocardial cell contraction and MH. To clarify, the PAC interacting protein and the cardiomyocyte function provide a theoretical basis for the pathology and treatment of hypertrophic cardiomyopathy.