Ross Andrea J, Tilman Christopher, Yao Humphrey, MacLaughlin David, Capel Blanche
Department of Cell Biology, Duke University Medical Center, Box 3709, 340 Nanaline Duke, Research Dr, Durham, NC 27710, USA.
Mol Cell Endocrinol. 2003 Dec 15;211(1-2):1-7. doi: 10.1016/j.mce.2003.09.021.
Migration of mesonephric cells into XY gonads is a critical early event in testis cord formation. Based on the fact that anti-Müllerian hormone (AMH) can induce testis cord formation in XX gonads, we investigated whether AMH plays a role in the induction of cell migration. Addition of recombinant AMH induced mesonephric migration into XX gonads in culture. AMH-treated XX gonads displayed increased vascular development and altered morphology of the coelomic epithelium, both features of normal testis differentiation. AMH did not induce markers of Sertoli or Leydig cell differentiation. We examined early testis development in Amh-deficient mice, but found no abnormalities, suggesting that any function AMH may have in vivo is redundant. Other transforming growth factor (TGF-beta) family proteins, bone morphogenetic proteins (BMP2 and BMP4) show similar inductive effects on XX gonads in culture. Although neither BMP2 nor BMP4 is expressed in embryonic XY gonads, our findings suggest that a TGF-beta signalling pathway endogenous to the XY gonad may be involved in regulation of mesonephric cell migration. The factors involved in this process remain to be identified.
中肾细胞迁移至XY性腺是睾丸索形成过程中关键的早期事件。基于抗苗勒管激素(AMH)可诱导XX性腺形成睾丸索这一事实,我们研究了AMH在诱导细胞迁移过程中是否发挥作用。添加重组AMH可诱导培养的中肾细胞迁移至XX性腺。经AMH处理的XX性腺显示出血管发育增加以及体腔上皮形态改变,这两者均为正常睾丸分化的特征。AMH并未诱导支持细胞或间质细胞分化标志物的出现。我们检查了Amh基因缺陷小鼠的早期睾丸发育情况,但未发现异常,这表明AMH在体内可能具有的任何功能都是多余的。其他转化生长因子(TGF-β)家族蛋白,即骨形态发生蛋白(BMP2和BMP4),对培养的XX性腺显示出类似的诱导作用。尽管BMP2和BMP4在胚胎XY性腺中均不表达,但我们的数据表明XY性腺内源性的TGF-β信号通路可能参与中肾细胞迁移的调控。这一过程中涉及的因子仍有待确定。