Expression of netrin-1 receptors in retina of oxygen-induced retinopathy in mice.
Expression of netrin-1 receptors in retina of oxygen-induced retinopathy in mice.
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DOI:
10.1186/1471-2415-14-102
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发表时间:
2014-08-22
影响因子:
2
通讯作者:
Xia XB
中科院分区:
文献类型:
--
作者:
Liu D;Xiong SQ;Shang L;Tian XF;Yang J;Xia XB
Netrin-1 has been reported to promote retinal neovascularization in oxygen-induced retinopathy (OIR). However, netrin-1 receptors, which may mediate netrin-1 action during retinal neovascularization, have not been characterized. In this study, we investigated netrin-1 receptor subtype expression and associated changes in the retinas of mice with OIR. C57BL/6J mice were exposed to 75±2% oxygen for 5 days and then returned to normal air to induce retinal neovascularization. Reverse transcriptase polymerase chain reaction (RT-PCR) and Western blot were used to examine the expression of netrin-1 receptor subtypes in the mouse retinas. Double staining of netrin-1 receptor subtypes and isolectin B4 was used to determine the location of the netrin-1 receptor subtypes in the retinas. Inhibition of retinal neovascularization was achieved by UNC5B shRNA plasmid intravitreal injection. Retinal neovascularization was examined by fluorescein angiography and quantification of preretinal neovascular nuclei in retinal sections. RT-PCR results showed that, except for UNC5A, netrin-1 receptor subtypes UNC5B, UNC5C, UNC5D, DCC, neogenin, and A2b were all expressed in the retinas of OIR mice 17 days after birth. Western blots showed that only UNC5B expression was significantly increased on that day, and immunofluorescence results showed that only UNC5B and neogenin were expressed in retinal vessels. Treatment of OIR mice with the UNC5B shRNA plasmid dramatically reduced neovascular tufts and neovascular outgrowth into the inner limiting membrane. UNC5B may promote retinal neovascularization in OIR mice.
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DOI:
10.1007/978-0-387-76715-4_2
发表时间:
2007-01-01
期刊:
AXON GROWTH AND GUIDANCE
影响因子:
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影响因子:
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通讯作者:
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DOI:
10.1016/j.biocel.2006.11.009
发表时间:
2007-01-01
影响因子:
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作者:
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通讯作者:
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