The trabecular meshwork (TM) tissue is responsible for maintaining the physiologic intraocular pressure (IOP) of the ocular globe. To perform this function the TM must rely on a variety of mechanisms. These mechanisms, acting either independently or in a coordinated manner, are governed by the expression of TM genes. Expression profiles of TM from adult intact tissue and infant cultured cells revealed the high level of diversity of the TM transcriptome, with only about 1% of its genes represented by more than 4 clones in any of the libraries. The profiles also revealed genes whose presence is associated with previously undescribed TM functions such the one that protects the TM tissue against calcification. These findings support the existence of numerous regulatory mechanisms in the TM and may help explaining the low percentage of glaucoma patients associated with each mutated glaucoma gene. Failure to maintain a physiological pressure can result in elevated IOP, a condition often associated with the development of glaucoma. Experimentally, different time-periods of an elevated pressure insult lead to the altered expression of distinct sets of genes. Thus, the ability of the TM to respond to mechanical and biochemical insults is possibly driven by induction or repression of a number of genes that, most likely, are different from those involved in regulation of normal IOP. None of the genes currently linked to glaucoma was present in the expression profile libraries whereas their expression in the TM was highly induced by effectors known to be causative of glaucomatous conditions. This analysis leads to the speculation that glaucoma candidate genes might be more related to genes responding to insults than to those involved in the maintenance of normal TM physiology. A recent study implicating the common stress mediator NF-kappaB in glaucoma would support this notion. Future library profiles utilizing distinct RNA sources together with differential expression studies between normal and glaucoma-triggering conditions and individual characterization of selected genes will help elucidate the relevant mechanisms for the regulation of IOP.

中文翻译：

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小梁网中的基因表达和眼压的影响。

小梁网（TM）组织负责维持眼球的生理性眼内压（IOP）。为了执行此功能，TM必须依靠多种机制。这些以独立或协调的方式起作用的机制受TM基因表达的支配。来自成年完整组织和婴儿培养细胞的TM表达谱显示TM转录组的高度多样性，在任何一个文库中，只有约1％的基因由4个以上的克隆代表。这些图谱还揭示了其存在与先前未描述的TM功能相关的基因，例如保护TM组织免于钙化的基因。这些发现支持TM中存在许多调节机制，并且可能有助于解释与每个突变的青光眼基因相关的青光眼患者的百分比低。无法维持生理压力会导致IOP升高，这通常与青光眼的发展有关。在实验中，高压损伤的不同时间段导致不同基因集的表达改变。因此，TM对机械和生化损伤的反应能力可能是由许多基因的诱导或抑制所驱动的，这些基因很可能与正常IOP调节所涉及的基因不同。表达谱库中目前没有与青光眼相关的基因，而它们在TM中的表达被已知是引起青光眼病的效应子高度诱导。这项分析导致推测，青光眼候选基因可能与对侮辱作出反应的基因比与维持正常TM生理的基因更为相关。最近一项涉及青光眼中常见的应激介质NF-κB的研究将支持这一观点。未来利用不同RNA来源的文库概况以及正常和青光眼触发条件之间的差异表达研究以及所选基因的个体表征将有助于阐明IOP调节的相关机制。这项分析导致推测，青光眼候选基因可能与对侮辱作出反应的基因比与维持正常TM生理的基因更为相关。最近一项涉及青光眼中常见的应激介质NF-κB的研究将支持这一观点。未来利用不同RNA来源的文库概况以及正常和青光眼触发条件之间的差异表达研究以及所选基因的个体表征将有助于阐明IOP调节的相关机制。这项分析导致推测，青光眼候选基因可能与对侮辱作出反应的基因比与维持正常TM生理的基因更为相关。最近一项涉及青光眼中常见的应激介质NF-κB的研究将支持这一观点。未来利用不同RNA来源的文库概况以及正常和青光眼触发条件之间的差异表达研究以及所选基因的个体表征将有助于阐明IOP调节的相关机制。