Akt3 is a target of miR-29c-3p and serves an important function in the pathogenesis of congenital heart disease

• Published in: International journal of molecular medicine 2019-02, Vol.43 (2), p.980
• Main Authors: Chen, Tao, Li, Shu-Jun, Chen, Bin, Huang, Qiong, Kong, Xiang-Ying, Shen, Chen, Gu, Hai-Tao, Wang, Xiao-Wei
• Format: Article
• Language: English
• Subjects: Apoptosis; Cancer; Cardiomyocytes; Cardiovascular disease; Care and treatment; Cell cycle; Cell growth; Congenital diseases; Congenital heart defects; Diagnosis; Gene expression; Genetic aspects; Genotype & phenotype; Health aspects; Heart; Kinases; MicroRNA; Polymerase chain reaction; Proteins; Studies; Womens health
• ISSN: 1107-3756; 1791-244X
• DOI: 10.3892/ijmm.2018.4008

Our previous studies identified that the expression of microRNA-29c (miR-29c-3p) was significantly increased in the serum of pregnant women carrying fetuses with congenital heart disease (CHD) compared with in that of normal pregnant women. However, the mechanism by which miR-29c-3p affects development of the embryonic heart remained unclear. The aim of the present study was to investigate the effect and potential molecular mechanism of miR-29c-3p overexpression on P19 cell proliferation, apoptosis and differentiation. miR-29c-3p-overexpression and protein kinase Bγ (Akt3)-knockdown cell lines were constructed using transfection technology. The function of miR-29c-3p and Akt3 in cardiomyocyte development was investigated by determining the proliferation, apoptosis and differentiation of P19 cells, which can differentiate into cardiomyocytes induced by dimethylsulfoxide. Bioinformatic analysis and luciferase assays were performed to explore the association between Akt3 and miR-29c-3p. The results of the present study revealed that miR-29c-3p overexpression and Akt3 knockdown suppressed proliferation, and promoted apoptosis and differentiation in P19 cells. Akt3 was also demonstrated to be a target of miR-29c-3p. Therefore, overexpression of miR-29c-3p may inhibit proliferation, and promote apoptosis and differentiation in P19 cells by inhibiting the expression of Akt3. miR-29c-3p may be a potential therapeutic target for the treatment of CHD.