GDNF stimulates the proliferation of cultured mouse immature Sertoli cells via its receptor subunit NCAM and ERK1/2 signaling pathway.
GDNF stimulates the proliferation of cultured mouse immature Sertoli cells via its receptor subunit NCAM and ERK1/2 signaling pathway.
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GDNF通过其受体亚基NCAM和ERK1/2信号通路刺激培养的小鼠未成熟支持细胞的增殖
DOI：
10.1186/1471-2121-11-78
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发表时间：
2010-10-18
期刊：
影响因子：
--
通讯作者：
Han C
中科院分区：
文献类型：
--
作者：
Yang Y;Han C
睾丸支持细胞的增殖和最终密度受激素和局部因素的调节。胶质细胞源性神经营养因子（Glial cell line-derived neurotrophic factor，GDNF）是转化生长因子-β超家族的一个远亲成员，其受体亚单位GDNF家族受体α 1（GFRα1）、RET酪氨酸激酶和神经细胞粘附分子（neural cell adhesion molecule，NCAM）在睾丸中表达，参与未成熟支持细胞（immature Sertoli cells，ISCs）增殖的调控。然而，这些受体亚基的表达模式和下游信号转导通路尚未在ISCs中得到解决。在本研究中，我们已经报道了培养的ISCs的增殖显着增强GDNF。ISCs表达GFRα1和NCAM受体亚单位，但不表达RET，抗NCAM抗体阻断或特异性靶向NCAM mRNA的siRNA可显著降低GDNF对ISCs增殖的刺激作用。此外，ERK 1/2抑制剂PD 98059完全消除GDNF对ISCs的促有丝分裂作用。GDNF通过其受体亚基NCAM和随后的ERK 1/2信号通路的激活来刺激ISCs的增殖。
The proliferation and final density of Sertoli cells in the testis are regulated by hormones and local factors. Glial cell line-derived neurotrophic factor (GDNF), a distantly related member of the transforming growth factor-β superfamily, and its receptor subunits GDNF family receptor alpha 1 (GFRα1), RET tyrosine kinase, and neural cell adhesion molecule (NCAM) have been reported to be expressed in the testis and involved in the regulation of proliferation of immature Sertoli cells (ISCs). However, the expression patterns of these receptor subunits and the downstream signaling pathways have not been addressed in ISCs. In the present study, we have reported that the proliferation of cultured ISCs was significantly enhanced by GDNF. The receptor subunits GFRα1 and NCAM but not RET were expressed in ISCs, and the stimulatory effect of GDNF on the proliferation of ISCs was significantly reduced by anti-NCAM antibody blocking or siRNA that specifically targets NCAM mRNA. Additionally, the ERK1/2 inhibitor, PD98059, completely abolished the mitogenic effect of GDNF on ISCs. GDNF stimulates the proliferation of ISCs via its receptor subunit NCAM and the consequent activation of the ERK1/2 signaling pathway.
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