[TGF-beta2 involvements in open angle glaucoma].

Clinica de Oftalmologie, Spitalul Clinic de Urgenţă Militar Central.
Oftalmologia (Bucharest, Romania: 1990) 02/2008; 52(3):110-2.
Source: PubMed


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.

0 Reads
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aqueous humour of patients with the senile cataract, cataract on the background of glaucoma and cataract on the background of glaucoma with pseudoexfoliative syndrome became a subject for immune enzyme analysis. Relatively high indices of fibronectin, insulin-like growth factor-1 and E2 prostaglandins were registered in aqueous humour of patients with the complicated cataracts compared to the same indices in senile cataracts. Due to the study performed, the role of fibroblasts transforming growth factor in the process of ACAID formation and withdrawal should be considered from a qualitatively new standpoint: in the aspect of its stimulatory influence on processes of selective synthesis of fibronectin and insulin-like growth factor-1 by cornea cells and the trabecular meshwork of the eye.In mechanism of ACAID withdrawal an important part should be assigned to E2 prostaglandins, as their high level in case of complicated cataracts might inhibit in situ activity of cytotoxic T-lymphocytes, thus facilitating activation of humoral immunity reactions in membranes of the eye.
    No preview · Article · Jan 2012 · New Armenian Medical Journal
  • Source
    [Show abstract] [Hide abstract]
    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.
    Full-text · Article · Sep 2012 · Investigative ophthalmology & visual science
  • [Show abstract] [Hide abstract]
    ABSTRACT: The given communication presents new data on the role of regional-mediatory mechanisms for formation and inhibition of immune reactions responsible for anterior chamber associated immune deviation (ACAID) making and course. Until nowadays, the opinion dominates in modern ophthalmology that at induction of in situ immune reactions responsible for ACAID formation at a wide range of eye diseases the key role is attributed to transforming growth factor (TGFβ-2) produced in eye membranes: cornea, ciliary body and trabecular meshwork. Furthermore, the entire cascade of in situ occurring immune reactions match the concept "ac-tive immunological tolerance" exceptionally connected with TGFβ-2 -dependent activation of cy-totoxic lymphocytes - in response to surgical trauma, as a result of which the antigenic determi-nants of damaged eye tissues are bared. On the basis of not numerous, but rather informative scientific data referring to the probable synthesis of a number of biological active compounds, which apart from their main functions pos-sess also the immunomodulatory specter of action (cortisol, prolactin, fibronectin and prostaglan-dins E2) in eye membranes, as well as based on our own long-term research findings we propose the concept, according to which the TGFβ-2-dependent mechanism is not the only one in induction of active immunological tolerance. To our mind, in ACAID induction and abolition mechanisms ear-lier unknown hormonal-mediatory mechanisms are also engaged, functioning in eye membranes on the principles of paracrine-autocrine reciprocal regulation and conditionality.
    No preview · Article · Jan 2013 · New Armenian Medical Journal
Show more