Open AccessStanozolol induces ventricular dysfunction by decreasing phospholamban phosphorylation in heart tissue of LDLr-/- mice
Author(s) -
Tadeu Uggere de Andrade,
Dionisio Dubois Fillho,
Cristiane Lyrio da Silva,
Mirian de Almeida Silva,
Simone Alves de Almeida,
Andrews Marques do Nascimento,
Nazaré Souza Bissoli,
Girlândia Alexandre Brasil,
Ewelyne Miranda de Lima
Publication year - 2022
Publication title -
research, society and development
Language(s) - English
Resource type - Journals
ISSN - 2525-3409
DOI - 10.33448/rsd-v11i5.27876
Subject(s) - phospholamban , stanozolol , medicine , ventricle , endocrinology , contractility , ventricular hypertrophy , muscle hypertrophy , phosphorylation , euthyroid , ldl receptor , left ventricular hypertrophy , cardiology , chemistry , heart failure , cholesterol , blood pressure , lipoprotein , hormone , biochemistry , anabolism
Stanozolol is a steroid that causes lipid deposition in LDLr-/- mice, although the mechanism by which this dyslipidemia results in cardiac dysfunction is little understood. The aim of this study was to evaluate the effect of stanozolol on cardiac contractility and the participation of myocardial phospholamban (pPLB) phosphorylation in an atherosclerosis mouse model. LDL receptor knockout mice (LDLr-/-) were fed a standard chow diet and received weekly subcutaneous injections of either saline (control, C group) or 20 mg/kg stanozolol (S group). After 8 weeks, hemodynamic parameters were assessed in the left ventricle. The heart was collected, weighted for hypertrophy evaluation, and kept in formalin buffer for morphometric analysis (H&E) and collagen quantification (Picrossirius). Protein expression of PLB and its phosphorylated form (p-PLB) in the left ventricle was determined by western blot. We observed that stanozolol treatment favored cardiac hypertrophy and collagen deposition in heart tissue. Also, stanozolol induced left ventricle dysfunction, increasing PBL expression and decreasing the p-PLB/PLB ratio. Altogether, our data showed that stanozolol causes cardiac remodeling and ventricular dysfunction by decreasing PLB phosphorylation in the left ventricle of LDLr-/- mice.