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      Quantitative relationships between transforming growth factor beta mRNA isoforms in congenital and traumatic cataracts

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          Abstract

          Purpose

          The aim of this study was to determine differences in the expression profiles of transforming growth factor ( TGF) β isoforms in the fragments of anterior lens capsules (ALCs) and peripheral blood mononuclear cells (PBMCs) of pediatric patients with congenital and traumatic cataracts.

          Methods

          Forty children with congenital cataracts (19 girls and 21 boys) and 22 children with traumatic cataracts (six girls and 16 boys) participated in the study. Fragments of ALCs obtained during cataract surgery and whole blood samples were analyzed. Quantification of TGFβ1, TGFβ2, and TGFβ3 mRNA was performed by real-time quantitative reverse transcription (QRT)-PCR using SYBR Green I chemistry.

          Results

          TGFβ1, TGFβ2, and TGFβ3 mRNA was detected in all the studied samples. Significant differences were found for TGFβ1 and TGFβ2 expression profiles in PBMCs between the patients with congenital and traumatic cataracts. The expression profiles of TGFβ isoforms in ALCs did not differ significantly between the groups.

          Conclusions

          Overexpression of TGFβ1 and TGFβ2 in the PBMCs of patients with congenital cataracts might indicate that these cytokines are involved in the development of lens opacity.

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          Most cited references42

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          Transforming growth factor-beta in human platelets. Identification of a major storage site, purification, and characterization.

          R Assoian, Blake Meyers, M. Sporn … (1983)
          Acidic ethanol extracts of human platelets induced non-neoplastic normal rat kidney fibroblasts to undergo anchorage-independent growth. Less than 100 ng/ml of the crude extract elicits 50% of the maximal biological response when assayed in the presence of epidermal growth factor (2.5 ng/ml). In the absence of epidermal growth factor, the potency of the extract decreased 1,000-fold. These results show that platelets contain a type beta transforming growth factor. The specific activity of the platelet extract is 100-fold greater than that of other non-neoplastic tissues. The growth factor was purified to homogeneity by sequential gel filtration on Bio-Gel P-60 columns, first in the absence and then in the presence of urea. As determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, this transforming growth factor-beta is a protein of 25,000 daltons. It is composed of two 12,500-dalton subunits held together by disulfide bonds. These results, as well as its amino acid composition and its lack of strong mitogenic activity, show that this protein is distinct from platelet-derived growth factor. When completely purified, transforming growth factor-beta elicits 50% of its maximal biological response at concentrations less than 5 x 10(-12) M.
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            miR-192 mediates TGF-beta/Smad3-driven renal fibrosis.

            Arthur Chung, Xiao R. Huang, Xiaoming Meng … (2010)
            TGF-beta/Smad3 promotes renal fibrosis, but the mechanisms that regulate profibrotic genes remain unclear. We hypothesized that miR-192, a microRNA expressed in the kidney may mediate renal fibrosis in a Smad3-dependent manner. Microarray and real-time PCR demonstrated a tight association between upregulation of miR-192 in the fibrotic kidney and activation of TGF-beta/Smad signaling. Deletion of Smad7 promoted miR-192 expression and enhanced Smad signaling and fibrosis in obstructive kidney disease. In contrast, overexpression of Smad7 to block TGF-beta/Smad signaling inhibited miR-192 expression and renal fibrosis in the rat 5/6 nephrectomy model; in vitro, overexpression of Smad7 in tubular epithelial cells abolished TGF-beta1-induced miR-192 expression. Furthermore, Smad3 but not Smad2 mediated TGF-beta1-induced miR-192 expression by binding to the miR-192 promoter. Last, overexpression of a miR-192 mimic promoted and addition of a miR-192 inhibitor blocked TGF-beta1-induced collagen matrix expression. Taken together, miR-192 may be a critical downstream mediator of TGF-beta/Smad3 signaling in the development of renal fibrosis.
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              Mechanisms of TGF-beta signaling in regulation of cell growth and differentiation.

              Aristidis Moustakas, Katerina Pardali, Annamaria Gaal … (2002)
              Transforming growth factor beta (TGF-beta) is a secreted protein that regulates proliferation, differentiation and death of various cell types. All immune cell lineages, including B, T and dendritic cells as well as macrophages, secrete TGF-beta, which negatively regulates their proliferation, differentiation and activation by other cytokines. Thus, TGF-beta is a potent immunosuppressor and perturbation of TGF-beta signaling is linked to autoimmunity, inflammation and cancer. Regulation of cell proliferation and differentiation by TGF-beta is a topic of great basic and clinical importance. We summarize our work on the growth inhibitory pathway downstream of TGF-beta, which is triggered by receptor serine/threonine kinases at the cell surface and downstream effectors of the Smad family. Activated Smads regulate transcription of target genes, including cell cycle inhibitors such as p21, which mediate the anti-proliferative response and partially explain the tumor suppressive action of the TGF-beta pathway. We have described a molecular mechanism of regulation of the p21 gene by Smads and transcription factor Sp1. At late stages of tumor progression, TGF-beta promotes tumorigenesis via suppression of the immune system and changes in cell differentiation of epithelial tumor cells, a phenomenon termed epithelial to mesenchymal transdifferentiation (EMT). We review our work on the role of the Smad pathway in controlling EMT. In conclusion, the molecular pathways that describe the anti-proliferative and transdifferentiating effects of TGF-beta in epithelial cells have been uncovered to great molecular detail; a future challenge will be to test their generality in other systems, including the immune system.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mol Vis
                Journal ID (publisher-id): MV
                Title: Molecular Vision
                Publisher: Molecular Vision
                ISSN (Electronic): 1090-0535
                Publication date Collection: 2011
                Publication date (Electronic): 18 November 2011
                Volume: 17
                Pages: 3025-3033
                Affiliations
                [1 ]Division of Pediatric Ophthalmology, Department of Ophthalmology, Medical University of Silesia, Katowice, Poland
                [2 ]Department of Molecular Biology, Medical University of Silesia, Sosnowiec, Poland
                Author notes

                The first two authors contributed equally to the work

                Correspondence to: Pawel Banasiak, Division of Pediatric Ophthalmology, Department of Ophthalmology, Medical University of Silesia, Ceglana 35 Street, 40-952 Katowice, Poland; Phone: +4832 3581277; FAX: +48 32 2518437; email: pawel.banasiak@ 123456gmail.com
                Article
                Publisher ID: 326 Publisher ID: 2011MOLVIS0166
                PMC ID: 3224844
                PubMed ID: 22128246
                SO-VID: 567d2693-0a57-460d-8302-d33c250c18c9
                Copyright © Copyright © 2011 Molecular Vision.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 12 April 2011
                Date accepted : 14 November 2011
                Categories
                Subject: Research Article
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                corr-author Banasiak

                ScienceOpen disciplines: Vision sciences
                Data availability:
                ScienceOpen disciplines: Vision sciences

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