Key result
Knockdown of junctophilin-2 in cultured rat cardiomyocytes decreased T-tubule regularity and the fraction of transverse elements, indicating JP2 is required for T-tubule morphogenesis.
Junctophilin-2 is essential for the structural maturation and morphogenesis of T-tubules in developing cardiomyocytes.
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Supports JP2 role in T-tubule maturation in vitro; hypothesis-generating for cardiomyopathy mechanisms, in vivo validation required before any clinical consideration.
The T-tubule (TT) system forms the structural basis for excitation-contraction coupling in heart and muscle cells. The morphogenesis of the TT system is a key step in the maturation of heart cells because it does not exist in neonatal cardiomyocytes. In the present study, we quantified the morphological changes in TTs during heart cell maturation and investigated the role of junctophilin-2 (JP2), a protein known to anchor the sarcoplasmic reticulum (SR) to TT, in changes to TT morphological parameters. Analysis of confocal images showed that the transverse elements of TTs increased, while longitudinal elements decreased during the maturation of TTs. Fourier transform analysis showed that the power of ∼2 μm spatial components increased with cardiomyocytes maturation. These changes were preceded by increased expression of JP2, and were reversed by JP2 knockdown. These findings indicate that JP2 is required for the morphogenesis of TTs during heart development.
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Han et al. (2013) studied Maturing cardiomyocytes. Junctophilin-2 (JP2) knockdown via shRNA adenovirus vs. Nonspecific sequence shRNA adenovirus (control) was evaluated on T-tubule regularity (TT power) and orientation (transverse vs longitudinal elements) (p=<0.01). Knockdown of junctophilin-2 in cultured rat cardiomyocytes decreased T-tubule regularity and the fraction of transverse elements, indicating JP2 is required for T-tubule morphogenesis.
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