Download PDF
Thromb Haemost 1999; 82(S 01): 23-26
DOI: 10.1055/s-0037-1615548
Commentaries
Schattauer GmbH

Control of Smooth Muscle Cell Proliferation – The Role of the Basement Membrane

Ulf Hedin
1   From the Department of Surgery, Division of Vascular Surgery, Karolinska Hospital, Stockholm, Sweden
,
Joy Roy
1   From the Department of Surgery, Division of Vascular Surgery, Karolinska Hospital, Stockholm, Sweden
,
Phan Kiet Tran
1   From the Department of Surgery, Division of Vascular Surgery, Karolinska Hospital, Stockholm, Sweden
,
Karin Lundmark
1   From the Department of Surgery, Division of Vascular Surgery, Karolinska Hospital, Stockholm, Sweden
,
Adnan Rahman
1   From the Department of Surgery, Division of Vascular Surgery, Karolinska Hospital, Stockholm, Sweden
› Author Affiliations Supported by grants from the Swedish Medical Research Council (12233), the Swedish Heart Lung Foundation, the Karolinska Institute, the King Gustav Vth 80th year fund, the Swedish-American Foundation, and the Swedish Institute.
Further Information

Publication History

Publication Date:
14 December 2017 (online)

Also available at
    Permissions and Reprints

Summary

In atherogenesis and in response to vessel injury, arterial smooth muscle cells (SMCs) are activated from a quiescent, differentiated state into an actively proliferating and synthetic phenotype which migrate into the intima where the cells participate in the formation of a fibrous plaque or intimal hyperplasia. The mechanisms involved in the control of SMC function are not clear and no preventive therapy against SMC activation is available. Interactions between SMCs and the extracellular matrix have been shown to influence SMC structure and function through integrin-mediated signaling processes. The SMC basement membrane is a specific form of extracellular matrix which seems to be crucial for the maintenance of SMC quiesence and the disruption of these interactions is part of cellular activation after atherogenic or traumatic stimuli. This concept of “negative growth control” may constitute a future target for the development of new strategies in the prevention of SMC activation in atherogenesis and restenosis formation.

Key words

Smooth muscle cells - restenosis - atherogenesis - cellular activation - basement membrane - integrins
 

  • References

  • 1 Thyberg J. Differentiated properties and proliferation of arterial smooth muscle cells in culture. Int Rev Cytol 1996; 169: 183-265.
    PubMedSearch in Google Scholar
  • 2 Hedin U, Clowes AW. Biology of vascular reconstructions: mechanisms of intimal hyperplasia, stenosis and restenosis. In Progress in Vascular Surgery. Eds Yao J. T., Pearce W. T.. Appelton and Lange; Chicago, Ill., USA: 37-50 1996
    Search in Google Scholar
  • 3 Risau W, Lemmon V. Changes of the vascular extracellular matrix during embryonic angiogenesis and vasculogenesis. Dev Biol 1988; 125: 441-50.
    CrossrefPubMedSearch in Google Scholar
  • 4 Thyberg J, Roy J, Tran PK, Hedin U. Phenotypic modulation of smooth muscle cells after arterial injury is associated with changes in the distribution of laminin and fibronectin. J Histochem Cytochem 1997; 45: 837-46.
    CrossrefPubMedSearch in Google Scholar
  • 5 Thyberg J, Blomgren K, Hedin U, Dryjski M. Phenotypic modulation of smooth muscle cells during the formation of neointimal thickenings in the rat carotid artery after balloon injury: an electronic-microscopic and stereological study. Cell Tissue Res 1995; 281: 421-8.
    CrossrefPubMedSearch in Google Scholar
  • 6 Hedin U, Bottger BA, Forsberg E, Johansson S, Thyberg J. Diverse effects of fibronectin and laminin on phenotypic properties of cultured arterial smooth muscle cells. J Cell Biol 1988; 107: 307-19.
    CrossrefPubMedSearch in Google Scholar
  • 7 Li X, Tsai P, Wieder ED, Kribben A, Van Putten V, Schrier RW, Nemenoff RA. Vascular smooth muscle cells grown on matrigel: a model of the contractile phenotype with decreased activation of mitogen-activated protein kinase. J Biol Chem 1994; 269: 19653-8.
    PubMedSearch in Google Scholar
  • 8 Hedin U, Thyberg J. Plasma fibronectin promotes modulation of arterial smooth muscle cells from contractile to synthetic phenotype. Differentiation 1987; 33: 239-46.
    CrossrefPubMedSearch in Google Scholar
  • 9 Reusch HP, Chan G, Ives HE, Nemenoff RA. Activation of JNK/SAPK and ERK by mechanical strain in vascular smooth muscle cells depends on extracellular matrix components. Biochem Biophys Res Comm 1997; 237: 239-44.
    CrossrefPubMedSearch in Google Scholar
  • 10 Reusch P, Wagdy H, Reusch R, Wilson E, Ives HE. Mechanical strain increases smooth muscle and decreases non muscle myosin expression in rat vascular smooth muscle cells. Circ Res 1996; 79: 1046-53.
    CrossrefPubMedSearch in Google Scholar
  • 11 Hynes RO. Integrins: versatility, modulation, and signaling in cell adhesion. Cell 1992; 69: 11-25.
    CrossrefPubMedSearch in Google Scholar
  • 12 Clark EA, Brugge JS. Integrins and signal transduction pathways: the road taken. Science 1995; 268: 233-9.
    CrossrefPubMedSearch in Google Scholar
  • 13 Lindner V, Lappi DA, Baird A, Majack RA, Reidy MA. Role of basic fibroblast growth factor in vascular lesion formation. Circ Res 1991; 68: 106-13.
    CrossrefPubMedSearch in Google Scholar
  • 14 Hedin U, Bottger BA, Johansson S, Thyberg J. A substrate of the cell attachment sequence of fibronectin (Arg-Gly-Asp-Ser) is sufficient to promote transition of arterial smooth muscle cells from a contractile to a synthetic phenotype. Dev Biol 1989; 133: 489-501.
    CrossrefPubMedSearch in Google Scholar
  • 15 Bottger BA, Hedin U, Johansson S, Thyberg J. Integrin-type fibronectin receptors of rat arterial smooth muscle cells: Isolation, partial characterization and role in cytoskeletal organization and control of differentiated properties. Differentiation 1989; 41: 158-67.
    CrossrefPubMedSearch in Google Scholar
  • 16 Hedin U, Sjˆlund M, HultgArdh-Nilsson A, Thyberg J. Changes in expression and organization of smooth muscle-specific a-actin during fibronectinmediated modulation of arterial smooth muscle cell phenotype. Differentiation 1990; 44: 222-31.
    CrossrefPubMedSearch in Google Scholar
  • 17 Hedin U, Thyberg J, Dumitrescu A, Roy J, Tran PK. Role of tyrosine phosphorylation in extracellular matrix mediated modulation of arterial smooth muscle cell phenotype. Arteriosclerosis Thromb Vasc Biol 1997; 17: 1977-84.
    CrossrefPubMedSearch in Google Scholar
  • 18 Hedin U, Daum G, Clowes AW. Disruption of integrin a5P1 signaling does not impair PDGF-BB-induced activation of extracellular-signal regulated kinase in smooth muscle cells. J Cell Physiol 1997; 172: 109-16.
    CrossrefPubMedSearch in Google Scholar
  • 19 Fang F, Orend G, Watanabe N, Hunter T, Ruoslahti E. Dependence of cyclin E-CDK2 kinase activity on cell anchorage. Science 1996; 271: 499-502.
    CrossrefPubMedSearch in Google Scholar
  • 20 Koyama H, Raines EW, Bornfeldt KE, Roberts JM, Ross R. Fibrillar collagen inhibits arterial smooth muscle cell proliferation through regulation of cdk2 inhibitors. Cell 1996; 87: 1069-78.
    CrossrefPubMedSearch in Google Scholar
  • 21 Assoian RK, Marcantonio EE. The extracellular matrix as a cell cycle control element in atherosclerosis and restenosis. J Clin Invest 1996; 98: 2436-9.
    CrossrefPubMedSearch in Google Scholar
  • 22 Weiser MC, Belknap JK, Grieshaber SS, Kinsella MG, Majack RA. Developmental regulation of perlecan gene expression in aortic smooth muscle cells. Matrix Biol 1996; 15: 331-40.
    CrossrefPubMedSearch in Google Scholar
  • 23 Weiser MC, Grieshaber SS, Schwartz PE, Majack RA. Perlecan regulates Oct-1 gene expression in vascular smooth muscle cells. Mol Biol Cell 1997; 8: 999-1011.
    CrossrefPubMedSearch in Google Scholar
  • 24 Clowes AW, Karnovsky MJ. Suppression by heparin of smooth muscle cell proliferation in injured arteries. Nature 1977; 265: 625-6.
    CrossrefPubMedSearch in Google Scholar
  • 25 Majesky MW, Schwartz SM, Clowes MM, Clowes AW. Heparin regulates smooth muscle S-phase entry in injured rat carotid artery. Circ Res 1987; 61: 296-304.
    CrossrefPubMedSearch in Google Scholar
  • 26 Lindner V, Olson NE, Clowes AW, Reidy MA. Inhibition of smooth muscle cell proliferation in injured rat arteries. Interaction of heparin with basic fibroblast growth factor. J Clin Invest 1992; 90: 2044-9.
    CrossrefPubMedSearch in Google Scholar
  • 27 Daum D, Hedin U, Wang T, Wang Y, Clowes AW. Diverse effects of heparin on mitogen-activated protein kinase-mediated signal transduction in vascular smooth muscle cells. Circulation Res 1997; 81: 17-23.
    CrossrefPubMedSearch in Google Scholar
  • 28 Hedin U, Daum G, Clowes AW. Heparin inhibits thrombin-induced mitogen-activated protein kinase signaling in baboon arterial smooth muscle cells. J Vasc Surg 1998; 27: 512-20.
    CrossrefPubMedSearch in Google Scholar
  • 29 Daub H, Weiss FU, Wallasch C. Ullrich : Role of transactivation of the EGF receptor in signalling by G-protein-coupled receptors. Nature 1996; 379: 557-60.
    CrossrefPubMedSearch in Google Scholar
  • 30 Reilly CF, Fritze LM, Rosenberg RD. Antiproliferative effects of heparin on vascular smooth muscle cells are reversed by epidermal growth factor. J Cell Physiol 1987; 131: 149-57.
    CrossrefPubMedSearch in Google Scholar