Overexpression of Na
Animals
Apoptosis
/ physiology
Bicarbonates
/ metabolism
Calcium
/ metabolism
Male
Mice
Mice, Transgenic
Myocardial Contraction
/ physiology
Myocardial Infarction
/ metabolism
Myocytes, Cardiac
/ metabolism
Sodium
/ metabolism
Sodium-Bicarbonate Symporters
/ metabolism
Ventricular Remodeling
/ physiology
Apoptosis
Calcium kinetics
Cardiac remodeling
Myocardial infarction
Sodium-bicarbonate ion transporter
Journal
Biochimica et biophysica acta. Molecular basis of disease
ISSN: 1879-260X
Titre abrégé: Biochim Biophys Acta Mol Basis Dis
Pays: Netherlands
ID NLM: 101731730
Informations de publication
Date de publication:
01 03 2020
01 03 2020
Historique:
received:
30
03
2019
revised:
25
10
2019
accepted:
22
11
2019
pubmed:
30
11
2019
medline:
4
8
2020
entrez:
29
11
2019
Statut:
ppublish
Résumé
The role of the cardiac isoform of the electrogenic sodium-bicarbonate ion cotransporter (NBCe1) in cardiac remodeling is not fully understood. The aim of this study was to assess the effects of NBCe1 overexpression on cardiac remodeling induced by myocardial infarction (MI) in mice. We generated NBCe1 transgenic (Tg) mice and NBCe1 overexpressing adult mouse ventricular myocytes (AMVMs) to investigate the role of NBCe1 on post-MI remodeling and calcium kinetics. Tg mice showed a markedly higher mortality rate and larger infarct size after MI. At 6 weeks after MI, the maximum rising rates of left ventricular pressure (dp/dt), contractility index, and the exponential time constant of relaxation (τ) were markedly lower, and there was higher cardiomyocyte apoptosis, in Tg mice compared with WT mice. In cultured AMVMs, overexpression of NBCe1 decreased sarcomere shortening and calcium amplitude. In WT AMVMs, the rates of the rise and decay phase of calcium transients, indicated by the rising time (T
Identifiants
pubmed: 31778748
pii: S0925-4439(19)30351-5
doi: 10.1016/j.bbadis.2019.165623
pii:
doi:
Substances chimiques
Bicarbonates
0
Sodium-Bicarbonate Symporters
0
Sodium
9NEZ333N27
Calcium
SY7Q814VUP
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
165623Informations de copyright
Copyright © 2019 The Authors. Published by Elsevier B.V. All rights reserved.