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      c-Myc antisense oligonucleotides preserve smooth muscle differentiation and reduce negative remodelling following rat carotid arteriotomy.

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          Abstract

          The vascular biology of restenosis is complex and not fully understood, thus explaining the lack of effective therapy for its prevention in clinical settings. The role of c-Myc in arteriotomy-induced stenosis, smooth muscle cell (SMC) differentiation and apoptosis was investigated in rat carotids applying full phosphorothioate antisense (AS) oligonucleotides (ODNs).

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          Mechanisms of apoptosis by c-Myc.

          G C Prendergast (1999)
          Much recent research on c-Myc has focused on how it drives apoptosis. c-Myc is widely known as a crucial regulator of cell proliferation in normal and neoplastic cells, but until relatively recently its apoptotic properties, which appear to be intrinsic, were not fully appreciated. Its death-dealing aspects have gained wide attention in part because of their potential therapeutic utility in advanced malignancy, where c-Myc is frequently deregulated and where novel modalities are badly needed. Although its exact function remains obscure, c-Myc is a transcription factor and advances have been made in characterizing target genes which may mediate its apoptotic properties. Candidate regulators and effectors are also emerging. Among recent findings are connections to the CD95/Fas and TNF pathways and roles for the tumor suppressor p19ARF and the c-Myc-interacting adaptor protein Binl in mediating cell death. In this review I summarize the data establishing a role for c-Myc in apoptosis in diverse settings and present a modified dual signal model for c-Myc function. It is proposed that c-Myc induces apoptosis through separate 'death priming' and 'death triggering' mechanisms in which 'death priming' and mitogenic signals are coordinated. Investigation of the mechanisms that underlie the triggering steps may offer new therapeutic opportunities.
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            Chimaeras of myc oncoprotein and steroid receptors cause hormone-dependent transformation of cells.

            D Picard, K. Yamamoto, K Eilers … (1989)
            The human proto-oncogene myc encodes a nuclear phosphoprotein whose primary biochemical function is still unknown. To facilitate further study of that function, we have created conditional alleles of myc by fusing the hormone-binding domain of the human oestrogen receptor gene to the 5' or the 3' end of human myc. The two chimaeric genes, designated mycer and ermyc, encode proteins that bind oestrogen with high affinity. Expression of one of the genes, mycer, transforms a rat fibroblast cell line in a tightly oestrogen-dependent manner. Transformation is dependent on the presence of a functional myc gene in the chimaera and is reversible upon removal of the hormone. The chimaeric genes will be useful tools to study the mechanisms by which Myc affects cellular phenotype. Recently, chimaeras between the adenovirus E1A protein and the hormone binding domain of the rat glucocorticoid receptor were shown to activate transcription in a manner characteristic for E1A, but in a hormone regulated manner. We therefore asked whether the same strategy could be applied to the product of myc.
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              Diverse contribution of bone marrow cells to neointimal hyperplasia after mechanical vascular injuries.

              Yasunobu Hirata, Masataka Sata, Kimie Tanaka … (2003)
              We and others have suggested that bone marrow-derived progenitor cells may contribute to the pathogenesis of vascular diseases. On the other hand, it was reported that bone marrow cells do not participate substantially in vascular remodeling in other experimental systems. In this study, three distinct types of mechanical vascular injuries were induced in the same mouse whose bone marrow had been reconstituted with that of GFP or LacZ mice. All injuries are known to cause smooth muscle cell (SMC) hyperplasia. At 4 weeks after wire-mediated endovascular injury, a significant number of the neointimal and medial cells derived from bone marrow. In contrast, marker-positive cells were seldom detected in the lesion induced by perivascular cuff replacement. There were only a few bone marrow-derived cells in the neointima after ligation of the common carotid artery. These results indicate that the origin of intimal cells is diverse and that contribution of bone marrow-derived cells to neointimal hyperplasia depends on the type of model.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): J. Vasc. Res.
                Title: Journal of vascular research
                Publisher: S. Karger AG
                ISSN: 1018-1172
                ISSN (Print): 1018-1172
                Publication date (Electronic): April 26 2005
                Volume: 42
                Issue: 3
                Affiliations
                [1 ] Excellence Research Center for Cardiovascular Diseases, Department of Experimental Medicine, Second University of Naples, Via Constantinopoli 16, IT-80138 Naples, Italy.
                Article
                Publisher Item ID: 85379
                DOI: 10.1159/000085379
                PubMed ID: 15849475
                SO-VID: 6a622dec-dfab-49f9-8b0b-d321caa6fdb2
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