Figure 2 | Scientific Reports

Figure 2

From: Aberrant Splicing Promotes Proteasomal Degradation of L-type CaV1.2 Calcium Channels by Competitive Binding for CaVβ Subunits in Cardiac Hypertrophy

Figure 2

Abundance of cardiac CaV1.2e21+22 channels is increased in mice in response to TAC surgery.

(A) Increased ratio of left ventricle to body weight in TAC mice. (B) Representative M-mode echocardiography images of mouse hearts before and 14 days after TAC surgery indicating progression of cardiac hypertrophy. (C) Increased LVAWd and LVPWd in TAC mice. (D) Representative gel photos for transcript screening of exons 21 + 22 inclusion level. Each lane represents a single colony expressing exons 21 + 22 or exon 21/22. (E) Inclusion level of exons 21 + 22 increased from 0.52% to 6.49% with the development of cardiac hypertrophy induced by pressure overload within 14 days (n = 6). (F–H) Expression levels of total CaV1.2 channels and CaVβ2 subunits in left ventricles (n = 8). (I,J) Ubiquitination level of cardiac CaV1.2 channels in left ventricles (n = 8). Data were shown as mean ± SEM. *p < 0.05, #p < 0.01. 1-way ANOVA was performed for multiple comparisons in panel E.

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