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Can J Physiol Pharmacol. 2017 Mar;95(3):305-309. doi: 10.1139/cjpp-2016-0570. Epub 2016 Nov 30.

Regulation of the cardioprotective adiponectin and its receptor AdipoR1 by salt.

Author information

1
a Department of Medicine, University of Missouri, Columbia, MO, USA.
2
b Harry S. Truman Memorial Veterans' Affairs Hospital, Columbia, MO, USA.
3
c Department of Biological Sciences, Mississippi State University, Starkville, MS, USA.
4
d Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO, USA.

Abstract

Both circulating adiponectin (APN) and cardiac APN exert cardioprotective effects and improve insulin sensitivity and mitochondrial function. Low circulating APN serves as a biomarker for cardiovascular risk. Ablation of adiponectin receptor 1 (AdipoR1) causes myocardial mitochondrial dysfunction. Although high salt intake is a contributor to cardiovascular disease, how it modulates the expression of APN or AdipoR1 in cardiomyocytes is not known. We report that APN mRNA expression was attenuated in a dose-dependent manner in mouse cardiomyocyte cell line HL-1 exposed to salt concentrations ranging from 0.75% to 1.5% for 12 h. High-salt exposure (0.88% and 1.25% for 12 h) also suppressed APN and AdipoR1 protein expression significantly in rat cardiac muscle H9c2 cells. Co-immunostaining for AdipoR1 and mitochondrial complex 1 indicated that AdipoR1 may be co-localized with mitochondria. These data show for the first time that high salt is an important suppressor of cardiovascular protective APN and AdipoR1.

KEYWORDS:

adiponectin; adiponectin receptor type 1; adiponectine; cardiovascular disease; maladie cardiovasculaire; récepteur de l’adiponectine de type 1; salt; sel

PMID:
28051329
PMCID:
PMC6372100
DOI:
10.1139/cjpp-2016-0570
[Indexed for MEDLINE]
Free PMC Article

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