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Regulation of the cardioprotective adiponectin and its receptor AdipoR1 by salt 1

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

Document Type: Research Article

Publication date: January 1, 2017

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