Skip to main content
. 2013 Jul 26;8(7):e70158. doi: 10.1371/journal.pone.0070158

Figure 8. miR-1 modulates Cx43 activity in cardiac hypertrophy.

Figure 8

A: cardiac levels of miR-1 after adenovirus-mediated cardiac overexpression in control saline-injected (Saline-Con) and in Iso-induced hypertrophic mice (Iso-LVH, *p<0.05 vs. Ad-Empty; #p<0.05 vs. Saline-Con). B: total and phosphorylated (Ser279/Ser282) Cx43 levels in normal and hypertrophic mouse hearts after Adeno-Empty or Adeno-miR-1 myocardial release (*p<0.05 vs. Ad-Empty; #p<0.05 vs. Saline-Con). C: immunohistochemistry and confocal microscopy in murine normal and hypertrophic heart sections; panels a-b show normal Cx43 expression in the gap junction (a) and very low level of its phosphorylation at Ser279/Ser282; ISO-induced LVH determined hyper-phosphorylation of Cx43 and its displacement from the gap junction to the cytoplasm of hypertrophic cardiomyocytes (c); panel d shows a significant reduction of phospho-Cx43 and its stabilization within the gap junction by adenovirus-mediated miR-1 selective intra-myocardial overexpression (red: α-sarcomeric actin, α-SA; green: Cx43 or p-Cx43; blue: DAPI).