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. 2021 Jun 15;12:678863. doi: 10.3389/fphys.2021.678863

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Copyright © 2021 Zhao, Ling, Zhong, Li, Li, Du, Jin, Zhao, Liu, Kan, Chang and Li.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Overexpression of CKIP-1 inhibits the phosphorylation of HDAC4. (A) Western blotting showing the expression levels of CKIP-1, phosphorylated HDAC4 (S632), phosphorylated HDAC4 (S246), and the total protein expression levels of HDAC4. (B) Quantification of p-HDAC4 (S632), p-HDAC4 (S246), and HDAC4 levels. (C–E) Transcript levels of hypertrophic marker genes (ANP, BNP, and β-MHC) in the hearts of WT and CKIP-1 TG mice after swimming exercise. Values are means ± SEM, n = 4∼6, ^∗P < 0.05, ^∗∗P < 0.01. Statistical differences among groups were analyzed by two-way analysis of variance (ANOVA) followed by the Bonferroni procedure. CKIP-1, casein kinase-2 interacting protein-1; WT, wild type; TG, transgenic; HDAC4, histone deacetylase 4; ANP, atrial natriuretic peptide; BNP, brain natriuretic peptide; β-MHC, myosin heavy chain β.