摘要
目的探讨TrkA、TrkC和p75NTR受体蛋白在激光损伤视网膜中的表达及意义。方法采用Wistar二级大鼠分别于532nm调Q倍频Nd:YAG激光损伤后12h、24h、3d、7d、14d、28d取眼球,用HE染色、免疫组织化学染色观察视网膜组织形态及TrkA、TrkC和p75NTR蛋白在激光损伤视网膜中的变化。结果TrkA、TrkC和p75NTR在激光损伤视网膜时均有表达,且呈动态变化。TrkA主要分布于视网膜内侧的节细胞核、M櫣ller细胞内侧端突起及内核层内侧端其他细胞(如双极细胞);TrkC主要分布于外核层,位于细胞浆中;p75NTR主要分布于外核层M櫣ller细胞外侧端突起。结论TrkA、TrkC和p75NTR受体表达参与激光损伤视网膜的病理过程。
Objective To investigate the effects of high-affinity tyrosine kinase receptors TrkA, TrkC and the low-affinity neurotrophin receptor p75 (p75~ NTR) protein in laser-induced retinal injury. Methods The Wistar rats were anesthetized and exposed to frequency doubling Neodymium:Yttrium,aluminum garnet(ND:YAG,λ=532nm) laser for 100 plus per eye, which were sacrificed on 12 hours,1,3,7,14 and 28 days after laser exposure and eyeball was taken out. We investigated retinal histology by hematoxylin and eosin staining, and the expression of TrkA, TrkC and p75~ NTR protein was studied by means of immunohistochemistry. Results Immunohistochemistry results showed a differential distribution for these three neurotrophin receptors in the laser injuried retina. TrkA was enhanced in nerve fiber layer (NFL), ganglion cell layer(GCL) and inner nuclear layer(INL) ,which is the most nuclei of the ganglion cells, proximal Müller cell end feet and a little cells in the innermost part of the INL, its peak of up-regulation was after day 1-3, after day 28 there was sustained. Whereas TrkC and p75~ NTR expression was enhanced in the outer nuclear layer(ONL), which is distal Müller cell processes, TrkC up-regulated after 12 hours, its peak was on day 1-3, after day 28 there was sustained, p75~ NTR up-regulated after 24 hours, its peak was on day 3, on day 14-28 there was sustained in the GCL, which is proximal Müller cell processes. Conclusion The expression of TrkA, TrkC and p75~ NTR participated in the course of laser injuried retinal pathology.
出处
《解放军医学杂志》
CAS
CSCD
北大核心
2005年第7期613-615,共3页
Medical Journal of Chinese People's Liberation Army
基金
全军医学科研"十五"规划指令性课题资助项目(编号01L020)