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Caveolin-3 KO Disrupts T-Tububle Structure and Decreases T-Tubular ICa Density in Mouse Ventricular Myocytes

Research output: Contribution to journalArticle

Original languageEnglish
Pages (from-to)H1101-H1111
Number of pages11
JournalAJP - Heart and Circulatory Physiology
Issue number5
Early online date20 Jul 2018
DateAccepted/In press - 11 Jul 2018
DateE-pub ahead of print - 20 Jul 2018
DatePublished (current) - Nov 2018


Caveolin-3 (Cav-3) is a protein that has been implicated in t-tubule formation and function in cardiac ventricular myocytes. In cardiac hypertrophy and failure, Cav-3 expression decreases, t-tubule structure is disrupted and excitation-contraction coupling (ECC) is impaired. However, the extent to which the decrease in Cav-3 expression underlies these changes is unclear. We therefore investigated the structure and function of myocytes isolated from the hearts of Cav-3 KO mice. These mice showed cardiac dilatation and decreased ejection fraction in vivo, compared to WT controls. Isolated KO myocytes showed cellular hypertrophy and altered t-tubule structure, and decreased L-type Ca channel (LTCC) current (ICa) density. This decrease in density occurred predominantly in the t-tubules, with no change in total ICa, and was therefore a consequence of the increase in membrane area. Cav-3 KO had no effect on LTCC expression, and C3SD peptide, which mimics the scaffolding domain of Cav-3, had no effect on ICa in KO myocytes. However, inhibiting protein kinase A using H-89 decreased ICa at the surface and t-tubule membranes in both KO and WT myocytes. Cav-3 KO had no significant effect on INCX or Ca release. These data suggest that Cav-3 KO causes cellular hypertrophy thereby decreasing t-tubular ICa density.
(200 words)

    Research areas

  • cavolin-3, calcium current, calcium transient, calcium release

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