Akt3 is a target of miR-29c-3p and serves an important function in the pathogenesis of congenital heart disease
Akt3 is a target of miR-29c-3p and serves an important function in the pathogenesis of congenital heart disease
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基于生物信息学方法识别人类椎间盘退变的潜在分子靶点
DOI：
10.3892/ijmm_xxxxxxxx
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发表时间：
2019
影响因子：
5.4
通讯作者：
XIAO-WEI WANG
中科院分区：
文献类型：
--
作者：
TAO CHEN;SHU-JUN LI;BIN CHEN;QIONG HUANG;XIANG-YING KONG;CHEN SHEN;HAI-TAO GU;XIAO-WEI WANG
摘要。我们前期研究发现，与正常孕妇相比，携带先天性心脏病（CHD）胎儿的孕妇血清中miR-29c-3p的表达明显升高。然而，miR-29c-3p影响胚胎心脏发育的机制尚不清楚。本研究旨在探讨miR-29c-3p过表达对P19细胞增殖、凋亡和分化的影响及其可能的分子机制。转染技术构建mir -29c-3p过表达和蛋白激酶Bγ (Akt3)敲低细胞系。通过检测二甲亚砜诱导的可向心肌细胞分化的P19细胞的增殖、凋亡和分化，探讨miR-29c-3p和Akt3在心肌细胞发育中的功能。采用生物信息学分析和荧光素酶测定来探讨两者之间的联系。Akt3和miR-29c-3p之间。本研究结果显示miR-29c-3p过表达和Akt3敲低可抑制P19细胞增殖，促进细胞凋亡和分化。Akt3也被证明是miR-29c-3p的靶标。因此，过表达miR-29c-3p可能通过抑制. akt3的表达抑制P19细胞的增殖，促进细胞凋亡和分化。miR-29c-3p可能是治疗冠心病的潜在治疗靶点。
Abstract. 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.