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Cardiomyocyte Proteome Remodeling due to Isoproterenol‐Induced Cardiac Hypertrophy during the Compensated Phase
Author(s) -
Parreira Ricardo Cambraia,
GómezMendoza Diana Paola,
Jesus Itamar Couto Guedes,
Lemos Rafael Pereira,
Santos Anderson Kennedy,
Rezende Cristiana Perdigão,
Figueiredo Henrique César Pereira,
Pinto Mauro Cunha Xavier,
Kjeldsen Frank,
Guatimosim Silvia,
Resende Rodrigo Ribeiro,
VeranoBraga Thiago
Publication year - 2020
Publication title -
proteomics – clinical applications
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.948
H-Index - 54
eISSN - 1862-8354
pISSN - 1862-8346
DOI - 10.1002/prca.202000017
Subject(s) - muscle hypertrophy , myh7 , heart failure , myocyte , medicine , downregulation and upregulation , cardiac myocyte , biology , microbiology and biotechnology , endocrinology , myosin , myosin light chain kinase , biochemistry , gene
Purpose Although the pathophysiological response of cardiac tissue to pro‐hypertrophic stimulus is well characterized, a comprehensive characterization of the molecular events underlying the pathological hypertrophy in cardiomyocytes during the early compensated cardiac hypertrophy is currently lacking. Experimental design A quantitative label‐free proteomic analysis of cardiomyocytes isolated was conducted from mice treated subcutaneously with isoproterenol (ISO) during 7 days in comparison with cardiomyocytes from control animals (CT). Results Canonical pathway analysis of dysregulated proteins indicated that ISO‐hypertrophy drives the activation of actin cytoskeleton and integrin‐linked kinase (ILK) signaling, and inhibition of the sirtuin signaling. Alteration in cardiac contractile function and calcium signaling are predicted as downstream effects of ISO‐hypertrophy probably due to the upregulation of key elements such as myosin‐7 (MYH7). Confocal microscopy corroborated that indeed ISO‐treatment led to increased abundance of MYH7. Potential early markers for cardiac hypertrophy as APBB1, GOLGA4, HOOK1, KATNA1, KIFBP, MAN2B2, and SLC16A1 are also reported. Conclusions and clinical relevance The data consist in a complete molecular mapping of ISO‐induced compensated cardiac hypertrophy model at cardiomyocyte level. Marker candidates reported may assist early diagnosis of cardiac hypertrophy and ultimately heart failure.