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      Inhibition of restenosis development after mechanical injury: a new field of application for malononitrilamides?

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          Abstract

          To investigate the efficacy of the malononitrilamide FK778 to prevent vascular smooth muscle cell (SMC) migration/proliferation, and vascular fibrosis, the key events in restenosis development using in vivo and in vitro studies.

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          Mechanisms of TGF-β Signaling from Cell Membrane to the Nucleus

          Yigong Shi, Joan Massagué (2003)
          Article 0 comments Cited 428 times – based on 0 reviews     Review now
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            In-Stent Restenosis: Contributions of Inflammatory Responses and Arterial Injury to Neointimal Hyperplasia

            Hongsheng Wu, Ran Kornowski, Mun Hong … (1998)
            Article 0 comments Cited 61 times – based on 0 reviews     Review now
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              Vasorin, a transforming growth factor beta-binding protein expressed in vascular smooth muscle cells, modulates the arterial response to injury in vivo.

              Y Ikeda, Y Imai, H. Kumagai … (2004)
              Growth factors, cell-surface receptors, adhesion molecules, and extracellular matrix proteins play critical roles in vascular pathophysiology by affecting growth, migration, differentiation, and survival of vascular cells. In a search for secreted and cell-surface molecules expressed in the cardiovascular system, by using a retrovirus-mediated signal sequence trap method, we isolated a cell-surface protein named vasorin. Vasorin is a typical type I membrane protein, containing tandem arrays of a characteristic leucine-rich repeat motif, an epidermal growth factor-like motif, and a fibronectin type III-like motif at the extracellular domain. Expression analyses demonstrated that vasorin is predominantly expressed in vascular smooth muscle cells, and that its expression is developmentally regulated. To clarify biological functions of vasorin, we searched for its binding partners and found that vasorin directly binds to transforming growth factor (TGF)-beta and attenuates TGF-beta signaling in vitro. Vasorin expression was down-regulated during vessel repair after arterial injury, and reversal of vasorin down-regulation, by using adenovirus-mediated in vivo gene transfer, significantly diminished injury-induced vascular lesion formation, at least in part, by inhibiting TGF-beta signaling in vivo. These results suggest that down-regulation of vasorin expression contributes to neointimal formation after vascular injury and that vasorin modulates cellular responses to pathological stimuli in the vessel wall. Thus, vasorin is a potential therapeutic target for vascular fibroproliferative disorders.
              Article 0 comments Cited 51 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Cardiology
                Title: Cardiology
                Publisher: S. Karger AG
                ISSN (Electronic): 1421-9751
                ISSN (Print): 0008-6312
                Publication date (Electronic): 2007
                Volume: 108
                Issue: 2
                Affiliations
                [1 ] Department of Cardiovascular Surgery, University Heart Center Hamburg, Hamburg, Germany.
                Article
                Publisher Item ID: 96037
                DOI: 10.1159/000096037
                PubMed ID: 17028423
                SO-VID: e41a6f68-8bfb-4d07-a95b-7db82841777b
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