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ATROPHIC CARDIOMYOCYTE SIGNALING IN HYPERTENSIVE HEART DISEASE.
MedLine Citation:
PMID:  24084216     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Cardinal pathologic features of hypertensive heart disease (HHD) include not only hypertrophied cardiomyocytes and foci of scattered microscopic scarring, a footprint of prior necrosis, but also small myocytes ensnared by fibrillar collagen where disuse atrophy with protein degradation would be predicted. Whether atrophic signaling is concordant with the appearance of HHD and involves oxidative and endoplasmic reticulum (ER) stress remains unexplored. Herein, we examine these possibilities focusing on the left ventricle (LV) and cardiomyocytes harvested from hypertensive rats receiving 4 wks aldosterone/salt treatment (ALDOST) alone or together with ZnSO4, a nonvasoactive antioxidant, with the potential to attenuate atrophy and optimize hypertrophy. Compared to untreated age-/sex-/strain-matched controls, ALDOST was accompanied by: a) LV hypertrophy with preserved systolic function; b) concordant cardiomyocyte atrophy (<1000 μm) found at sites bordering on fibrosis where they were re-expressing β-myosin heavy chain; and c) upregulation of ubiquitin ligases, MuRF1 and atrogin-1, and elevated 8-isoprostane and unfolded protein ER response with mRNA upregulation of stress markers. ZnSO4 cotreatment reduced lipid peroxidation, fibrosis and the number of atrophic myocytes, together with a further increase in cell area and width of atrophied and hypertrophied myocytes, and improved systolic function, but did not attenuate elevated blood pressure. We conclude that atrophic signaling, concordant with hypertrophy, occurs in the presence of a reparative fibrosis and induction of oxidative and ER stress at sites of scarring where myocytes are atrophied. ZnSO4 cotreatment in HHD with ALDOST attenuates the number of atrophic myocytes, optimizes size of atrophied and hypertrophied myocytes, and improves systolic function.
Authors:
German Kamalov; Wenyuan Zhao; Tieqiang Zhao; Yao Sun; Robert A Ahokas; Tony N Marion; Fahed Al Darazi; Ivan C Gerling; Syamal K Bhattacharya; Karl T Weber
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2013-9-30
Journal Detail:
Title:  Journal of cardiovascular pharmacology     Volume:  -     ISSN:  1533-4023     ISO Abbreviation:  J. Cardiovasc. Pharmacol.     Publication Date:  2013 Sep 
Date Detail:
Created Date:  2013-10-2     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7902492     Medline TA:  J Cardiovasc Pharmacol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
1Division of Cardiovascular Diseases 2Department of Obstetrics & Gynecology 3Department of Microbiology, Immunology and Biochemistry 4Division of Endocrinology, University of Tennessee Health Science Center, Memphis, TN.
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