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首页> 外文期刊>Journal of Cellular Physiology >Genes expressed in the human trabecular meshwork during pressure-induced homeostatic response.
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Genes expressed in the human trabecular meshwork during pressure-induced homeostatic response.

机译：基因表达在人类小梁网在pressure-induced稳态响应。

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摘要

Physiological pressure inside the eye is maintained by a resistance mechanism provided by the trabecular meshwork tissue. In most cases, prolonged, elevated pressure leads to an eye pathology characterized by retinal ganglion cell (RGC) degeneration, optic nerve damage, and non-remedial blindness. We are investigating the regulation of trabecular meshwork genes in response to elevated pressure. Using perfused organ cultures from postmortem human donors, we have previously demonstrated the presence of a homeostatic mechanism at 2-4 days of pressure insult (Borras et al. 2002, Invest Ophthalmol Vis Sci 43:33-40). Here, we sought to identify trabecular meshwork genes whose expression was altered during this homeostatic period. By macroarray hybridization, we compared the expression profiles of high-pressure (HP) and normal-pressure (NP) treated eyes from the same individual (n = 3 pairs). Our results identified 40 upregulated and 14 downregulated genes. The highest proportion of upregulated genes encoded proteins involved in signal transduction (32%). Among the potentially relevant genes, PIP 5K1C, VIP, tropomodulin, and MMP2 encoded mediators known to influence outflow resistance. Others encoded functions which are new for the trabecular meshwork, but which are intrinsic to unrelated tissues. These new mechanisms appear as they could be of benefit for trabecular meshwork function. Matrix Gla protein (MGP), perlecan, osteomodulin, and osteoblast-specific factor are essential in cartilage and bone physiology whereas spectrin and ICAM4 are specific for blood cells and crucial in maintaining their shape and adhesion. In addition, MGP transcripts were stimulated by extracellular calcium and downregulated by TGF-beta1. We propose that MGP might be an important player in the adaptive homeostatic mechanism by contributing to maintain a softer trabecular meshwork tissue and facilitate aqueous humor outflow. J. Cell. Physiol. 201: 126-137, 2004. Copyright 2004 Wiley-Liss, Inc.
机译：生理压力在眼睛里面耐药机制提供的维护小梁网组织。长时间,压力升高导致病理表现为视网膜神经节细胞(RGC)变性、视神经的损害non-remedial失明。小梁网基因的调控应对压力升高。从后期人类捐赠者器官文化,我们之前展示的存在吗体内平衡机制在2 - 4天的压力侮辱(Borras et al . 2002年,投资角膜切削力Sci 43:33-40)。小梁网基因的表达在这段自我平衡的改变。macroarray杂交,我们比较了高压(惠普)和表达谱正常压力(NP)眼睛从相同的对待个人(n = 3双)。40调节和14个基因表达下调。最高比例的调节基因编码蛋白质参与信号转导(32%)。潜在的相关基因中,皮普5 k1c,贵宾,tropomodulin, MMP2介质进行编码已知流出阻力的影响。编码的新功能小梁网,但固有的不相关的组织。他们可能是小梁网的好处函数。osteomodulin, osteoblast-specific因素在软骨和骨骼生理至关重要而血影蛋白和ICAM4特定流人的血在保持其形状和细胞和至关重要的附着力。由细胞外钙和刺激由TGF-beta1表达下调。可能是自适应的一个重要球员有助于保持体内平衡机制一个温和的小梁网组织促进房水外流。杂志。201:126 - 137年,2004年。Wiley-Liss公司。

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