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P. Russell, X. Zhao, K.E. Pearson, D.A. Stephan; Effects of Prostaglandin Analogues on Human Ciliary Muscle and Trabecular Meshwork Cells . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4233.
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Purpose: To discover genes that might increase aqueous humor outflow when human ciliary muscle (CM) or human trabecular meshwork (TM) cells are treated with prostaglandin F2α analogues. Methods: Cultures of CM and TM cells from five donors were treated with 10µg/ml of either latanoprost free acid or prostaglandin F2α ethanolamide (prostamide) for nine days. The mRNAs from the cells were analyzed with Affymetrix U95Av2 microarrays and the result confirmed with relative quantitative PCR. Results: About one dozen mRNAs had a two-fold or greater change. Both latanoprost and prostamide gave similar results in each cell types. Four genes that changed expression would appear to be candidates to alter outflow. In the CM, aquaporin 1 and versican were both decreased, but remained unchanged in the TM. In contrast, fibroleukin and IGF-1 were increased in the TM but not altered in the CM. Two other genes upregulated in the TM were promelanosome concentrating hormone and tumor necrosis factor-10 (TRAIL). Conclusions: Aquaporin-1 knockout animals have decreased IOP, thus the reduction in mRNA for this gene could increase outflow. The decrease in versican in the CM might change the glycoaminoglycan composition around the CM and increase outflow. The secretion of the protease, fibroleukin, could alter the extracellular matrix of TM. Changes in IGF-1 reported to increase metalloproteinases could increase facility; however, increasing IGF-1 might have other effects. Similarly, the promelanosome concentrating hormone, apart from influencing pigmentation, has profound effects on metabolism. TRAIL has not been previously reported in the TM and its role is uncertain.
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