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血小板衍生生长因子-BB 和表皮生长因子通过 Ras/ERK1/2 信号通路促进奶山羊精原干细胞增殖。

Platelet-derived growth factor-BB and epidermal growth factor promote dairy goat spermatogonial stem cells proliferation via Ras/ERK1/2 signaling pathway.

机构信息

Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi, 712100, China.

School of Life Science and Biotechnology, Shanghai Jiao Tong University, Shanghai, 200240, China.

出版信息

Theriogenology. 2020 Oct 1;155:205-212. doi: 10.1016/j.theriogenology.2020.06.012. Epub 2020 Jun 22.

Abstract

Spermatogonial stem cells (SSCs) have been used for the production of transgenic animals and for the recovery of male fertility. However, the proliferation of SSCs in vitro is still immature, and the mechanisms and pathways involved in the proliferation of SSCs are not clear. Here, the effects of platelet-derived growth factor-BB (PDGF-BB) and epidermal growth factor (EGF) on the proliferation of dairy goat SSCs in vitro were detected. The results showed that 20 ng/ml PDGF-BB or 25 ng/ml EGF was the optimum concentration, and that the BCL2 in the experimental groups was significantly higher than that in the control (P < 0.05), while BAX and BAD were dramatically downregulated (P < 0.05). The pERK1/2 in the experimental groups was about 3-5 times higher than that in the control. After the specific MEK1/2 inhibitor was added, BCL2 was reduced significantly (P < 0.001), while BAX and BAD were upregulated (P < 0.001). The expression of pERK1/2 decreased by 10%-30%. We speculated that these two growth factors may be mediated through the Ras/ERK1/2 signaling pathway to regulate the expression of pERK1/2 protein, and thus enhance the resistance of SSCs to apoptosis. However, further studies are needed to verify this hypothesis.

摘要

精原干细胞(SSCs)已被用于生产转基因动物和恢复雄性生育力。然而,SSCs 在体外的增殖仍然不成熟,并且参与 SSCs 增殖的机制和途径尚不清楚。在这里,检测了血小板衍生生长因子-BB(PDGF-BB)和表皮生长因子(EGF)对体外奶山羊 SSCs 增殖的影响。结果表明,20ng/ml PDGF-BB 或 25ng/ml EGF 是最佳浓度,实验组的 BCL2 明显高于对照组(P<0.05),而 BAX 和 BAD 则显著下调(P<0.05)。实验组的 pERK1/2 约为对照组的 3-5 倍。添加特定的 MEK1/2 抑制剂后,BCL2 明显减少(P<0.001),而 BAX 和 BAD 上调(P<0.001)。pERK1/2 的表达降低了 10%-30%。我们推测这两种生长因子可能通过 Ras/ERK1/2 信号通路介导,调节 pERK1/2 蛋白的表达,从而增强 SSCs 对细胞凋亡的抵抗力。然而,需要进一步的研究来验证这一假设。

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