Expression of heat shock proteins in the monkey eyes

1.热休克蛋白在灵长类青光眼视网膜中的表达用氩激光反复照射房角造成实验性青光眼模型。用免疫组化方法检测HSPs的表达，结果显示，与正常对照组相比，HSP90，60，27在青光眼视网膜中表达明显增加，提示HSP90，60，27在青光眼视网膜中具有神经保护作用。HSP70在青光眼视网膜中也有中度升高。HSP47的表达对视网膜细胞外基质的重塑起着重要作用.用ZeissDAB分析系统定量分析，除HSP47.2外，其他HSP分子均发生了显著变化。热休克蛋白在灵长类实验性青光眼视神经乳头的表达除HSP 47外，其他HSP视神经乳头的表达均减少。免疫组化结果显示，筛板中HSP 47和70表达增强。原位杂交也证实了HSP70和47在筛板的表达增加。结论：与筛板前和筛板后区相比，筛板区HSP表达增加，可能在筛板区的结构重建中起重要作用，HSP可能在青光眼神经病变的发病机制中起重要作用。HSP在青光眼视网膜和视神经乳头的表达存在差异，HSP的作用有待于进一步研究，以确定控制HSP的表达是否能成为青光眼神经保护的一种治疗方案。

1. Expression of Heat Shock Protein in the primate glaucomatous retinaExperimental glaucoma model was made by repeated exposure of argon laser to the chamber angle. Intraocular pressure and optic nerve head was then monitored.Immunohistochemistry was performed for panels of antibodies against HSPs.Neuroprotective HSP (90,60,27) were upregulated in the glaucomatous retina compared with that of control normal retina. HSP 70 was also moderately elevated in the glaucomatous retina. Expression of HSP 47, act to extracellular material remodeling was not altered in glaucomatous retina. Such immunoreactivity was quantificated by Zeiss DAB analysis system and significantly change was obtained for all HSP molecules except that of HSP 47.2. Expression of Heat Shock Protein in the optic nerve heads of primate experimental glaucoma.Expression of HSP was decreased in the optic nerve head in all HSP except for HSP 47. In lamina cribrosa, HSP 47 and 70 showed enhanced expression by immunohistochemistry. In situ hybridization also demonstrated increased expression of HSP 70 and 47 at lamina cribrosa. Lamina cribrosa, contrast to prelamina and retro laminal portion, showed increased expression of HSP may indicate important role for the remodeling of this specific area, which is believed to play an important role for glaucomatous neuropathy.As a summary, HSP may play an important role for the pathogenesis of glaucomatous neuropathy. Expression of HSP was different between retina and optic nerve head in glaucomatous eyes.Further study should be warranted to clear the role of HSP for future possibility whether controlling the HSP expression become neuroprotective regimen for glaucomatous neuropathy.