Key result
Thoracic aortic banding-induced cardiac hypertrophy was much less prominent in transgenic mice overexpressing an NCX1 mutant with defective phosphorylation sites compared to controls.
Why the study?
Does NCX1 phosphorylation contribute to load-induced cardiac hypertrophy in vivo?
Does NCX1 phosphorylation contribute to load-induced cardiac hypertrophy in vivo?
The phosphorylation status of NCX1 plays a critical role in the development of load-induced cardiac hypertrophy in vivo.
Answers are grounded in this paper and cite their sources.
NCX1 phosphorylation may mediate load-induced hypertrophy; animal data leave open human relevance and therapeutic targeting.
Both protein kinase Calpha-dependent Na+/Ca2+ exchanger1 (NCX1) phosphorylation and calcineurin activity are required for the depression of NCX activity observed in chronically phenylephrine (PE)-treated hypertrophic neonatal rat cardiomyocytes. In this study, we explored the possibility that the same changes occur in vivo hypertrophy. In the hypertrophic hearts of thoracic aortic-banded (TAB) mice, NCX1 phosphorylation increased significantly compared with control hearts. Furthermore, the TAB-induced cardiac hypertrophy was much less prominent in transgenic mice overexpressing an NCX1 mutant having defective phosphorylation sites. These data suggest that the phosphorylation status of NCX1 may play an important role in the pathogenesis of load-induced cardiac hypertrophy.
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Katanosaka et al. (2007) studied Cardiac hypertrophy. Thoracic aortic banding (TAB) and NCX1 mutant overexpression vs. Control hearts / wild-type mice was evaluated on NCX1 phosphorylation and cardiac hypertrophy. Thoracic aortic banding-induced cardiac hypertrophy was much less prominent in transgenic mice overexpressing an NCX1 mutant with defective phosphorylation sites compared to controls.
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