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MMP2-TIMP2 system and primary open-angle glaucoma correlation
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MMP2/TIMP2 system and primary open-angle glaucoma correlation
[Abstract] Objective 2 matrix metalloproteinase / tissue inhibitor of metalloproteinase 2 (MMP 2/TIMP 2) system in primary open angle glaucoma may pathogenesis. Methods 20 normal human cadaver eyes, medium primary open angle glaucoma 20 eyes with advanced primary open-angle glaucoma 22 eyes underwent trabeculectomy, was detected by RT PCR trabecular meshwork tissue MMP 2 mRNA and TIMP 2 mRNA expression. Results normal and in advanced primary open-angle glaucoma trabecular meshwork both MMP 2 mRNA and TIMP 2 mRNA expression, MMP 2 mRNA in normal human trabecular meshwork was highly expressed in primary open angle glaucoma was significantly lower, and the disease develops gradually reduce its expression, TIMP 2 mRNA was low in the normal expression of the trabecular meshwork in primary open angle glaucoma was significantly increased, and with the progression and its expression gradually increased, primary open-angle glaucoma trabecular MMP 2 mRNA / TIMP 2 mRNA were significantly lower than normal, and the ratio gradually decreases with the progression. Conclusion trabecular meshwork extracellular matrix TIMP exception of MMP inhibition, resulting in system imbalance MMP 2/TIMP 2 , may be the primary open-angle glaucoma pathogenesis.
[Keywords:] primary open-angle glaucoma, trabecular meshwork, extracellular matrix, matrix metalloproteinase 2, matrix metalloproteinase inhibitor 2
Primary open-angle glaucoma (primary open angle glaucoma, POAG) is a common blinding eye disease, to date, its etiology and pathogenesis is unclear. Now that the resistance of the trabecular meshwork to increase aqueous discharge induced intraocular pressure is the main reason for optic nerve damage caused by POAG. trabecular meshwork endothelial cells called the extracellular matrix of sediment (extracellular maxtrix, ECM), the trabecular cells in maintaining the normal outflow of aqueous humor
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