Notch signaling inhibition induces G0/G1 arrest in murine Leydig cells
Notch signaling inhibition induces G0/G1 arrest in murine Leydig cells
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Notch 信号传导抑制诱导小鼠 Leydig 细胞 G0/G1 停滞
DOI：
10.1111/and.13413
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发表时间：
2019-09-15
期刊：
影响因子：
2.4
通讯作者：
Zhang, Chunping
中科院分区：
文献类型：
--
作者：
Lu, Enhang;Feng, Fen;Zhang, Chunping
Notch作为一种进化上高度保守的信号通路，广泛参与细胞命运的决定和各种组织器官的发育。在男性生殖中，Notch信号通路的研究主要集中在生殖细胞和支持细胞。睾丸间质细胞是睾酮的主要生产者，在精子发生和维持第二性征中起着重要作用。本研究以小鼠睾丸间质细胞系TM 3细胞为研究对象，探讨Notch受体和配体的表达谱，并观察Notch信号对TM 3细胞增殖的影响。结果表明，Notch 1-3及其配体Dll-1和Dll-4在TM 3细胞中表达，Notch 1-3及其配体Dll-1在睾丸间质细胞中表达，抑制Notch信号通路可抑制TM 3细胞的增殖并诱导G 0/G1期阻滞。Notch信号传导的抑制增加了p21（Waf 1/Cip 1）和p27的表达。总之，我们的研究结果表明，Notch抑制TM 3细胞和P21（Waf 1/Cip 1）的增殖，和p27可能有助于这一过程。
As a highly evolutionarily conserved signaling pathway, Notch widely participates in cell-fate decisions and the development of various tissues and organs. In male reproduction, research on the Notch signaling pathway has mainly concentrated on germ cells and Sertoli cells. Leydig cells are the primary producers of testosterone and play important roles in spermatogenesis and maintaining secondary sexual characteristics. In this study, we used TM3 cells, a murine adult Leydig cell line, to investigate the expression profiles of Notch receptors and ligands and observe the effect of Notch signaling on the proliferation of TM3 cells. We found that Notch 1-3 and the ligands Dll-1 and Dll-4 were expressed in TM3 cells, Notch 1-3 and the ligand Dll-1 were expressed in testis interstitial Leydig cells, and Notch signaling inhibition suppressed the proliferation of TM3 cells and induced G0/G1 arrest. Inhibition of Notch signaling increased the expression of p21(Waf1/Cip1) and p27. Overall, our results suggest that Notch inhibition suppresses the proliferation of TM3 cells and P21(Waf1/Cip1), and p27 may contribute to this process.