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      The Controversial Role of TGF-β in Neovascular Age-Related Macular Degeneration Pathogenesis

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          Abstract

          The multifunctional transforming growth factors-beta (TGF-βs) have been extensively studied regarding their role in the pathogenesis of neovascular age-related macular degeneration (nAMD), a major cause of severe visual loss in the elderly in developed countries. Despite this, their effect remains somewhat controversial. Indeed, both pro- and antiangiogenic activities have been suggested for TGF-β signaling in the development and progression of nAMD, and opposite therapies have been proposed targeting the inhibition or activation of the TGF-β pathway. The present article summarizes the current literature linking TGF-β and nAMD, and reviews experimental data supporting both pro- and antiangiogenic hypotheses, taking into account the limitations of the experimental approaches.

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          Matricellular proteins: extracellular modulators of cell function.

          Paul Bornstein, E.Helene Sage (2002)
          The term 'matricellular' has been applied to a group of extracellular proteins that do not contribute directly to the formation of structural elements in vertebrates but serve to modulate cell-matrix interactions and cell function. Our understanding of the mode of action of matricellular proteins has been advanced considerably by the recent elucidation of the phenotypes of mice that are deficient in these proteins. In many cases, aspects of these phenotypes have illuminated previously unsuspected consequences of the lack of appropriate interactions of cells with their environment.
          Article 0 comments Cited 217 times – based on 0 reviews     Review now
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            Laser-induced choroidal neovascularization model to study age-related macular degeneration in mice.

            María de la Luz Guerrero-González, Jean-Michel Foidart, Vincent Lambert … (2013)
            The mouse model of laser-induced choroidal neovascularization (CNV) has been used extensively in studies of the exudative form of age-related macular degeneration (AMD). This experimental in vivo model relies on laser injury to perforate Bruch's membrane, resulting in subretinal blood vessel recruitment from the choroid. By recapitulating the main features of the exudative form of human AMD, this assay has served as the backbone for testing antiangiogenic therapies. This standardized protocol can be applied to transgenic mice and can include treatments with drugs, recombinant proteins, antibodies, adenoviruses and pre-microRNAs to aid in the search for new molecular regulators and the identification of novel targets for innovative treatments. This robust assay requires 7-14 d to complete, depending on the treatment applied and whether immunostaining is performed. This protocol includes details of how to induce CNV, including laser induction, lesion excision, processing and different approaches to quantify neoformed vasculature.
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              Structural Biology and Evolution of the TGF-β Family.

              Andrew Hinck, Thomas Mueller, Timothy Springer (2016)
              We review the evolution and structure of members of the transforming growth factor β (TGF-β) family, antagonistic or agonistic modulators, and receptors that regulate TGF-β signaling in extracellular environments. The growth factor (GF) domain common to all family members and many of their antagonists evolved from a common cystine knot growth factor (CKGF) domain. The CKGF superfamily comprises six distinct families in primitive metazoans, including the TGF-β and Dan families. Compared with Wnt/Frizzled and Notch/Delta families that also specify body axes, cell fate, tissues, and other families that contain CKGF domains that evolved in parallel, the TGF-β family was the most fruitful in evolution. Complexes between the prodomains and GFs of the TGF-β family suggest a new paradigm for regulating GF release by conversion from closed- to open-arm procomplex conformations. Ternary complexes of the final step in extracellular signaling show how TGF-β GF dimers bind type I and type II receptors on the cell surface, and enable understanding of much of the specificity and promiscuity in extracellular signaling. However, structures suggest that when GFs bind repulsive guidance molecule (RGM) family coreceptors, type I receptors do not bind until reaching an intracellular, membrane-enveloped compartment, blurring the line between extra- and intracellular signaling. Modulator protein structures show how structurally diverse antagonists including follistatins, noggin, and members of the chordin family bind GFs to regulate signaling; complexes with the Dan family remain elusive. Much work is needed to understand how these molecular components assemble to form signaling hubs in extracellular environments in vivo.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 27 October 2018
                Publication date Collection: November 2018
                Volume: 19
                Issue: 11
                Electronic Location Identifier: 3363
                Affiliations
                [1 ]Ophthalmology Unit of the Department of Medicine, Surgery and Neuroscience, University of Siena, Siena 53100, Italy; gmtosi18@ 123456gmail.com
                [2 ]Department of Biotechnology, Chemistry and Pharmacy, University of Siena, Siena 53100, Italy
                Author notes
                [* ]Correspondence: maurizio.orlandini@ 123456unisi.it (M.O.); federico.galvagni@ 123456unisi.it (F.G.); Tel.: +39-0577-234961 (F.G.)
                Author information
                https://orcid.org/0000-0003-1967-9554
                Article
                Publisher ID: ijms-19-03363
                DOI: 10.3390/ijms19113363
                PMC ID: 6275040
                PubMed ID: 30373226
                SO-VID: a82e5620-339c-4af3-9510-26aabf822a54
                Copyright © © 2018 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 12 October 2018
                Date accepted : 25 October 2018
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: neovascular age-related macular degeneration (namd),tgf-β,angiogenesis,choroidal neovascularization (cnv)
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: neovascular age-related macular degeneration (namd), tgf-β, angiogenesis, choroidal neovascularization (cnv)

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