Genetic Mechanisms Contribute to the Development of Heart Failure in Patients with Atrioventricular Block and Right Ventricular Apical Pacing

Figures

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  Figure 1. Nuclear location of Lamin A/C by fluorescence microscope. (A) The WT NRCMs showed regular rounded nucleus and lamin A/C demonstrated as small aggregates homogenously distributed in the nucleus envelope; (B) Lamin A/C mutations (R216C and L379F) showed nucleus with irregular shape (→), lamin A/C appeared profoundly impaired, clearly expressed in highlighted aggregates of different sizes, not uniformly distributed along the nucleus envelope.

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  Figure 2. No significant differences on the location and expression of Nav1.5 or Cx43 between Lamin A/C WT and mutations. (A) Western blot showed equal expression level of Nav1.5 and Cx43; (B,C) Confocal imaging did not reveal significant difference on the expression either in nucleic membrane or in cytomembrane. ns, not significant.

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  Figure 3. Apoptotic rate assessed by TUNEL and Western blot detection of activated caspase 3 in normally cultured and serum starved Lamin A/C NRCMs. (A) Confocal imaging of TUNEL assay showing normally cultured Lamin WT, R216C and L379 had similar apoptotic rate. HoweverLamin A/C R216C and L379F with serum starvation had significantly increased apoptotic rate. (B) Quantification of apoptotic rate was valued. (C) After serum starvation, there is no significant difference in the expression level of activated caspase 3.*p-value < 0.05; ns, not significant.