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All Journal The Avicenna Medical Journal
Rajarajan A Thandavarayan
Houston Methodist DeBakey Heart and Vascular Center, 6550 Fannin Street, Houston, TX 77030, USA
Biochemistry, Genetics & Molecular Biology Health Professions Immunology & microbiology Medicine & Pharmacology Public Health

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Potential Protective Role of 14-3-3 Protein in Pathological Cardiac Hypertrophy Through The Regulation of Endoplasmic Reticulum Stress: Role of Calreticulin Flori R. Sari; Rajarajan A Thandavarayan; Vivian Soetikno
The Avicenna Medical Journal Vol 2, No 2 (2021)
Publisher : Faculty of Medicine, UIN (State Islamic University) Syarif Hidayatullah Jakarta

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.15408/avicenna.v2i2.25441

Abstract

Introduction: 14-3-3 protein plays an important role in protecting cardiac cells from hypertrophy and endoplasmic reticulum stress during pressure overload elicited by aortic banding (AB) surgery; however, the relation among these protective roles is largely unknown. Methods: We investigated the in vivo role of 14-3-3 protein in two protocols involving C57/BL-6 mice and dominant negative (DN) 14-3-3η mice subjected to three- or seven-days pressure overload stimulation by applying AB surgery. The protein expressions of cardiac hypertrophy and ER stress markers, including atrial natriuretic peptide (ANP), galectin-3, glucose-regulated protein (GRP)78, calreticulin as well as 14-3-3 protein was analyzed by western blot. Results: Three- or seven-day pressure overload stimulation significantly increased the heart weight/body weight (HW/BW) ratio; cardiomyocyte diameter; and the protein expression levels of ANP, GRP78 as well as 14-3-3 in the C57/BL-6 mice. Partial inactivation of 14-3-3 protein in the DN 14-3-3η mice significantly increased the protein expression of ANP, Galectin-3, GRP78, and calreticulin after three- or seven-days AB surgery. Conclusion: These results suggest that 14-3-3 protein, as a molecular chaperone, protects against pathological cardiac hypertrophy, at least in part, by maintaining the normal ER function through the regulation of GRP78 and calreticulin.
Co-Authors Flori R. Sari Vivian Soetikno