Knockdown of bone morphogenetic protein 4 gene induces apoptosis and inhibits proliferation of bovine cumulus cells

文献类型: 外文期刊

第一作者: Tian, Ya-Qing

作者: Tian, Ya-Qing;Wang, Wan-Jie;Hao, Hai-Sheng;Zou, Hui-Ying;Pang, Yun-Wei;Zhao, Xue-Ming;Zhu, Hua-Bin;Du, Wei-Hua;Li, Xiao-Li

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关键词: Bone morphogenetic protein 4; Bovine cumulus cells; Apoptosis; Cell proliferation; Cell cycle

期刊名称:THERIOGENOLOGY ( 影响因子:2.923; 五年影响因子:2.843 )

ISSN: 0093-691X

年卷期: 2022 年 188 卷

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收录情况: SCI

摘要: The expression and function of bone morphogenetic protein 4 (BMP4) gene in bovine cumulus cells (CCs) was investigated to reveal the mechanisms by which it regulated cell apoptosis and proliferation. The mRNA and protein expression of BMP4 were detected using quantitative PCR (qPCR) and immunofluo-rescence staining in CCs. The effective siRNAs against BMP4 gene were screened using qPCR and western blotting. The mRNA expression levels of apoptosis-related genes and proliferation-related genes were estimated by qPCR after knocking-down the BMP4 gene in bovine CCs. Cell apoptosis, proliferation and cell cycle were measured with Annexin V-FITC, CCK-8 and propidium iodide staining by flow cytometry. Results showed that the BMP4 gene was expressed and its protein was in the cytoplasm and nuclei of bovine CCs. The BMP4 knockdown increased the cell apoptosis rate and upregulated the mRNA levels of apoptosis genes CASPASE-3 and BAX with downregulation of the anti-apoptosis gene BCL-2 (P < 0.05). The proliferation rate declined and the mRNA expression levels of proliferation-related genes PCNA, CDC42 and CCND2 were downregulated in the bovine CCs with BMP4 low expression (P < 0.05). The BMP4 knockdown significantly increased the percentage of G0/G1 phase cells while decreased that of S phase cells. Therefore, the expression of BMP4 and its biological functions on the cell proliferation, apoptosis and cell cycle of bovine CCs were first studied. BMP4 knockdown induced cell apoptosis, cell cycle arrest and inhibited proliferation of bovine CCs. (c) 2022 Elsevier Inc. All rights reserved.

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