Effect of overexpression of aldehyde dehydrogenase family member A2 on hypertrophic growth and proliferation of cardiomyocytes.

Hang LIU; Qiqi LIU; Zhenhua LI; Xiao YANG; Jian WANG

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Effect of overexpression of aldehyde dehydrogenase family member A2 on hypertrophic growth and proliferation of cardiomyocytes.

Author: Hang LIU ¹ ; Qiqi LIU ² ; Zhenhua LI ² ; Xiao YANG ¹ ; Jian WANG ²
Author Information

1. Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Anhui Medical University, Hefei 230000, Anhui, China.
2. National Center for Protein Sciences (Beijing), Academy of Military Medical Sciences, Beijing 100850, China.
Publication Type:Journal Article
Keywords: Aldh1a2; adenovirus; cardiac hypertrophy; cardiomyocyte proliferation
MeSH: Myocytes, Cardiac/cytology*; Animals; Cell Proliferation; Aldehyde Dehydrogenase 1 Family/metabolism*; Rats; Retinal Dehydrogenase/metabolism*; Adenoviridae/metabolism*; Cells, Cultured; Rats, Sprague-Dawley; Cardiomegaly/metabolism*; Up-Regulation; Aldehyde Dehydrogenase, Mitochondrial
From: Chinese Journal of Biotechnology 2024;40(12):4660-4669
CountryChina
Language:Chinese
Abstract: Retinoic acid signaling pathway plays a role in regulating vertebrate development, cell differentiation, and homeostasis. As a key enzyme that catalyzes the oxidation of retinal to retinoic acid, aldehyde dehydrogenase 1 family member A2 (Aldh1a2) is involved in cardiac development, while whether it functions in heart diseases remains to be studied. In this study, we infected primary cardiomyocytes with adenovirus overexpressing Aldh1a2 (Ad-Aldh1a2) to explore the effects of Aldh1a2 overexpression on the biological function of cardiomyocytes. The results showed that the infection with Ad-Aldh1a2 realized the overexpression of Aldh1a2 in cardiomyocytes. Compared with the control group infected with Ad-GFP, the cardiomyocytes infected with Ad-Aldh1a2 showcased significantly increased size and up-regulated expression levels of the atrial natriuretic factor gene (ANF), brain natriuretic peptide gene (BNP), and β-myosin heavy chain (β-MHC). In addition, 5-ethynyl-2'-deoxyuridine (EdU) incorporation assay demonstrated that Aldh1a2 overexpression increased the proportion of cardiomyocytes with positive EdU signals and upregulated the expression levels of proliferation-related genes cyclin D2 (Ccnd2) and budding uninhibited by benzimidazole 1 (Bub1). The above data indicated that overexpression of Aldh1a2 induced hypertrophic growth and proliferation of cardiomyocytes. This study provides a basis for further understanding the function of Aldh1a2 in heart diseases and developing therapies for heart diseases.