Destructive Role of TMAO in T-Tubule and Excitation-Contraction Coupling in the Adult Cardiomyocytes.

Abstract:

:Heart failure (HF) is a disease with high morbidity and mortality. In patients with HF, decreased cardiac output and blood redistribution results in decreased intestinal perfusion and destruction of intestinal barrier. Microorganisms and endotoxins can migrate into the blood circulation, aggravating systemic inflammation and HF. Trimethylamine N-oxide (TMAO) is highly closed to the occurrence of HF. However, the exact mechanism between TMAO and HF remains unclear.To investigate the role of TMAO in transverse-tubule (T-tubule) in the cultured cardiomyocytes.T-tubule imaging and analysis detected T-tubule network in cardiomyocytes. Ca2+ handling dysfunction was identified by confocal Ca2+ imaging. Tubulin densification and polymerization were assessed by western blot and immunofluorescent staining of cardiomyocytes.TMAO induced T-tubule network damage in cardiomyocytes and Ca2+ handling dysfunction in cardiomyocytes under the TMAO stress via promoting tubulin densification and polymerization and therefore Junctophilin-2 (JPH2) redistribution. Mice treated with TMAO represented cardiac dysfunction and T-tubule network disorganization.TMAO impairs cardiac function via the promotion of tubulin polymerization, subsequent translocation of JPH2, and T-tubule remodeling, which provides a novel mechanism for the relationship between HF and elevated TMAO.

journal_name

Int Heart J

authors

Jin B,Ji F,Zuo A,Liu H,Qi L,He Y,Wang Q,Zhao P

doi

10.1536/ihj.19-372

subject

Has Abstract

pub_date

2020-03-28 00:00:00

pages

355-363

issue

2

eissn

1349-2365

issn

1349-3299

journal_volume

61

pub_type

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