title: Regulation of the cardioprotective adiponectin and its receptor AdipoR1 by salt.
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.
authors.affiliation: a Department of Medicine, University of Missouri, Columbia, MO, USA.|b Harry S. Truman Memorial Veterans' Affairs Hospital, Columbia, MO, USA.
authors.forename: Nicholas
authors.initials: N
authors.lastname: Arnold
authors.affiliation: a Department of Medicine, University of Missouri, Columbia, MO, USA.|b Harry S. Truman Memorial Veterans' Affairs Hospital, Columbia, MO, USA.
authors.forename: Abuzar
authors.initials: A
authors.lastname: Mahmood
authors.affiliation: c Department of Biological Sciences, Mississippi State University, Starkville, MS, USA.
authors.forename: Maya
authors.initials: M
authors.lastname: Ramdas
authors.affiliation: a Department of Medicine, University of Missouri, Columbia, MO, USA.|b Harry S. Truman Memorial Veterans' Affairs Hospital, Columbia, MO, USA.
authors.forename: Paul P
authors.initials: PP
authors.lastname: Ehlinger
authors.affiliation: a Department of Medicine, University of Missouri, Columbia, MO, USA.|b Harry S. Truman Memorial Veterans' Affairs Hospital, Columbia, MO, USA.|d Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO, USA.
authors.forename: Lakshmi
authors.initials: L
authors.lastname: Pulakat
mesh_terms: D052242:Adiponectin / Q000235:genetics / Q000378:metabolism*; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D002460:Cell Line; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation; D051379:Mice; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D054419:Receptors, Adiponectin / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects; D012965:Sodium Chloride / Q000494:pharmacology*
chemical_list: D052242:Adiponectin; C499919:Adipoq protein, mouse; C499920:Adipoq protein, rat; D012333:RNA, Messenger; D054419:Receptors, Adiponectin; C475419:adiponectin receptor 1, mouse; C504339:adiponectin receptor 1, rat; D000804:Angiotensin II; D012965:Sodium Chloride
keywords: adiponectin; adiponectin receptor type 1; adiponectine; cardiovascular disease; maladie cardiovasculaire; récepteur de l’adiponectine de type 1; salt; sel