[TGF-beta2 involvements in open angle glaucoma].
ABSTRACT To emphasize the correlation between TGF beta2 and primary open angle glaucoma (POAG).
Observational clinical study on two groups of patients: group I--17 patients with POAG who need surgical approach and group II--16 patients without glaucoma. The groups were homogeneous regarding age and sex. The exclusion criteria were any associated systemic pathology. The concentration of TGF beta2 in the aqueous humor of each patient of both groups was measured by ELISA method.
After the comparative analysis we observed that TGF beta2 was more increased in patients with POAG than in patients without the disease. The changes of trabecular extra cellular matrix are induced by many factors. TGF beta2 is a special cytokine witch is believed to increase the fibronectin concentration in the trabecular meshwork and alter the extra cellular matrix turn-over with a final profibrotic effect.
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ABSTRACT: To compare follistatin (FST) and activin (Act) expression in normal and glaucomatous trabecular meshwork (TM) cells and tissues and determine if exogenous TGF-β2 regulates the expression of FST and Act in TM cells. Total RNA was isolated from TM cell strains, and mRNA expression for FST 317/344 isoforms and Act was determined via RT-PCR and quantitative PCR (qPCR). Western immunoblotting and immunocytochemistry determined FST and Act A protein levels in normal TM (NTM) and glaucomatous TM (GTM) cells. Cells were treated with recombinant human TGF-β2 protein at 0 to 10 ng/mL for 0 to 72 hours. qPCR, Western immunoblotting, immunocytochemistry, and ELISA immunoassay were utilized to determine changes in FST and Act A mRNA and protein levels. In addition, NTM and GTM tissue samples were examined by immunohistochemistry for expression of FST, FST 315, FST 288, and Act A. Both FST mRNA and protein levels were significantly elevated in GTM cells. FST mRNA transcripts FST 317/344 were also significantly elevated in GTM cells. Immunohistochemistry showed FST levels were significantly elevated in GTM tissues. Exogenous TGF-β2 significantly induced FST mRNA and protein expression. Immunohistochemistry demonstrated that Act A protein levels were significantly higher in NTM tissues compared to GTM tissues. FST is elevated in GTM cells and tissues. FST is known to be an inhibitor of bone morphogenetic proteins (BMPs), which, coupled with the ability of TGF-β2 to upregulate FST levels, may indicate a possible role of FST in the pathogenesis of glaucoma. These results suggest that additional endogenous molecules in human TM may regulate TGF-β2 signaling via inhibition of BMP family members.Investigative ophthalmology & visual science 09/2012; 53(11):7358-69. DOI:10.1167/iovs.12-10292 · 3.66 Impact Factor