当前位置： SCI文献检索 > BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS期刊下所有文献 > Different roles of β-arrestin and the PKA pathway in mitochondrial ROS production induced by acute β-adrenergic receptor stimulation in neonatal mouse cardiomyocytes.

Different roles of β-arrestin and the PKA pathway in mitochondrial ROS production induced by acute β-adrenergic receptor stimulation in neonatal mouse cardiomyocytes.

Abstract：

:Reactive oxygen species (ROS) play a crucial role in various physiological and pathological processes mediated by β-adrenergic receptors (β-ARs) in cardiomyocytes. However, the sources and signaling pathways involved in ROS production induced by acute β-AR activation have not yet been fully defined. In primary neonatal mouse cardiomyocytes (NMCMs), the β-AR agonist isoproterenol (ISO) induced a rapid increase in mitochondrial ROS and total ROS production. Both the expression and activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2/4 (NOX 2/4) remained unchanged after 2 h of ISO treatment, suggesting that acute ISO stimulation mainly induces mitochondrial ROS production in NMCMs. Knockdown of β-arrestin1, but not β-arrestin2, inhibited ISO-induced mitochondrial ROS production within 1-2 h after ISO treatment. Moreover, forskolin, an adenylyl cyclase (AC) activator, rapidly increased mitochondrial ROS as early as 15 min after ISO treatment. Inhibition of the cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) pathway abolished the mitochondrial ROS production within 15-60 min after ISO treatment. In conclusion, mitochondria are the major source of ROS production upon acute ISO stimulation. β-arrestin1, but not β-arrestin2, is involved in ISO-induced mitochondrial ROS production. Upon acute β-AR stimulation in NMCMs, the classical cAMP/PKA pathway is responsible for faster mitochondrial ROS production, whereas β-arrestin1 signaling is responsible for slower mitochondrial ROS production.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Zhang J,Xiao H,Shen J,Wang N,Zhang Y

doi

10.1016/j.bbrc.2017.05.140

subject

Has Abstract

pub_date

2017-08-05 00:00:00

pages

393-398

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(17)31040-9

journal_volume

489

pub_type

杂志文章

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