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. 2019 Mar 18;10:235. doi: 10.3389/fphys.2019.00235

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Copyright © 2019 Samal, Evangelista, Galang, Srivastava, Zhao and Vedantham.

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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MiR-1 Negatively Regulates VCS Proliferation and Cdk-6 Protein Expression. (A) Phosphohistone H3 staining in WT and miR-1 TG hearts at E12.5 shows a reduction in PH3+ cells in transgenic animals as compared to WT. The graph shows the percentage of trabecular nuclei that are PH3+ in each genotype. “^∗∗∗” denotes p < 0.001. (B) Co-staining of phosphohistone H3 and beta-galactosidase in Irx3-LacZ and Irx3-LacZ; MiR-1 TG E12.5 hearts demonstrates reduced mitotic index specifically in the developing VCS. The graph shows the percentage of beta-galactosidease nuclei that are also phosphohistone H3 positive “^∗∗∗” denotes p < 0.001. (C) mRNA level of Cdk6 is unchanged in postnatal hearts from miR-1 TG versus WT littermates, while protein level is significantly decreased, consistent with translational regulation. Knockdown of miR-1 in HL-1 cells results in upregulation of Cdk6 at the protein level. ^∗ denotes p < 0.05.