Skip to main content
. 2015 Dec 30;291(8):4128–4143. doi: 10.1074/jbc.M115.689620

FIGURE 5.

FIGURE 5.

Biomechanical stress causes junctional remodeling in mice lacking myozap. Electron micrographs showing the ID structure of wild-type (A, panels I and II) and myozap-KO (B, panels I and II) mice after TAC indicating disorganized IDs. Light microscopy images of wild-type (A, panel III) and myozap-KO (B, panel III) mice after TAC exhibiting cardiomyocyte degeneration in myozap-KO mice. Expression of intercalated disc proteins that directly or indirectly interact with myozap was determined by Western blotting and showed strong up-regulation of desmoplakin and desmin (C–E), although N-cadherin, connexin-43 (F–H), and ZO-1 (I and J) were strongly reduced after the induction of biomechanical stress due to TAC in Mzp−/− mice. Expression of Nav1.5 was unaltered in mice or rat cardiomyocytes (K–N), whereas connexin-43 was again down-regulated after myozap knockdown in stressed or unstressed cardiomyocytes (M and O). n = 6. Statistical significance was calculated by two-way ANOVA. Error bars show mean ± S.E. *, p < 0.05; **, p < 0.01; ***, p < 0.001.