The deletion of Math5 disrupts retinal blood vessel and glial development in mice
详细信息查看全文 | 推荐本文 |
摘要
Retinal vascular development is a complex process that is not yet fully understood. The majority of research in this area has focused on astrocytes and the template they form in the inner retina, which precedes endothelial cells in the mouse retina. In humans and dogs, however, astrocyte migration follows behind development of blood vessels, suggesting that other cell types may guide this process. One such cell type is the ganglion cell, which differentiates before blood vessel formation and lies adjacent to the primary retinal vascular plexus. The present study investigated the potential role played by ganglion cells in vascular development using m>Math5m>m>鈭?鈭?/em> mice. It has previously been reported that m>Math5m> regulates the differentiation of ganglion cells and m>Math5m>m>鈭?鈭?/em> mice have a 95%reduction in these cells. The development of blood vessels and glia was investigated using m>Griffonia simplicifoliam> isolectin B4 labeling and GFAP immunohistochemistry, respectively. JB-4 analysis demonstrated that the hyaloid vessels arose from choriovitreal vessels adjacent to the optic nerve area. As previously reported, m>Math5m>m>鈭?鈭?/em> mice had a rudimentary optic nerve. The primary retinal vessels did not develop post-natally in the m>Math5m>m>鈭?鈭?/em> mice, however, branches of the hyaloid vasculature eventually dove into the retina and formed the inner retinal capillary networks. An astrocyte template only formed in some areas of the m>Math5m>m>鈭?鈭?/em> retina. In addition, GFAP+ M眉ller cells were seen throughout the retina that had long processes wrapped around the hyaloid vessels. Transmission electron microscopy confirmed M眉ller cell abnormalities and revealed disruptions in the inner limiting membrane. The present data demonstrates that the loss of ganglion cells in the m>Math5m>m>鈭?鈭?/em> mice is associated with a lack of retinal vascular development.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700