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. 2020 Feb 21;12(4):3126–3139. doi: 10.18632/aging.102668

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Copyright © 2020 Xu et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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MG53 knockdown reversed the effect of AK045171 on cardiac hypertrophy. (A, B) qPCR was used to evaluate the efficiency of adenoviruses used to induce AK045171 overexpression or knockdown in myocardium and the expression of MG53. (C, D) HE staining of the heart under TAC, TAC+Ad-AK045171, TAC+ shRNA and TAC+sh-MG53 treatment. TAC significantly elevated the level of AK045171 in cardiomyocytes and myocardium. (E) The echoradiographic parameters LVEDP, LVFS, LVEF, and LVESD in mice were evaluated with an ultrasound system. (F) Quantification of heart weight-to-tibial length ratio. (G, H) qPCR was used to evaluate the efficiency of adenoviruses used for AK045171 overexpression and knockdown in cultured cardiomyocytes and the expression of MG53 (I) The level of the myocardial hypertrophy biomarkers ANP, BNP and β-MHC were detected using qPCR. (J) Immunostaining of α-SMA was used to evaluate the size of cardiomyocytes subjected to AngII, AngII+Ad-AK045171, AngII+Ad-AK045171+shRNA or AngII+Ad-AK045171+sh-MG53 treatment.*p<0.05 vs TAC or Ang II group; ^# p<0.05 vs TAC+Ad-AK054171+si-nc or Ang II+Ad-AK054171+si-nc group.