Abstract
The accumulation of vascular smooth muscle cells (VSMCs) in neointima resulting from the migration and proliferation of medial VSMCs in response to end-othelial damage is believed to be one of the main events involved in the initiation of atherosclerosis. Although various types of growth factor and cytokines, including endothelin-1 (ET-1), platelet-derived growth factor-B (PDGF-B) and angiotensin II (Ang II), have been acknowledged to contribute generally to the development of atherosclerosis, recent studies have indicated that many species of oxidants can be considered to be early growth signals.1,2
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsPreview
Unable to display preview. Download preview PDF.
References
A.S. Baas and B.C. Berk, Differential activation of mitogen-activated protein kinases by H2O2 and O2- in vascular smooth muscle cells, Circ. Res. 11, 29–36 (1995).
G.N. Rao and B.C. Berk, Active oxygen species stimulate vascular smooth muscle cell growth and proto-oncogene expression, Circ. Res. 70, 593–599 (1992).
T. Morita, M.A. Perrella, M.E. Lee, and S. Kourembanas, Smooth muscle cell-derived carbon monoxide is a regulator of vascular cGMP, Proc. Natl. Acad. Sci. USA. 92, 1475–1479 (1995).
T. Morita, S.A. Mitsialis, Y. Liu, and S. Kourembanas, Carbon monoxide controls the proliferation of hypoxic vascular smooth muscle cells, J. Biol. Chem. 52, 32804–32809 (1997).
T. Morita and S. Kourembanas, Endothelial expression of vasoconstrictors and growth factors is regulated by smooth muscle cell-derived carbon monoxide, J. Clin. Invest. 96, 2676–2682 (1995).
A.W. Clowes, M.A. Reidy, and M.M. Clowes, Kinetics of cellular proliferation after arterial injury, I: smooth muscle growth in the absence of endothelium, Lab. Invest. 49, 327–333 (1983).
N. Goda, K. Suzuki, M. Naito, S. Takeoka, E. Tsuchida, Y. Ishimura, T. Tamatani, and M. Suematsu, Distribution of heme oxygenase isozymes in rat liver, J. Clin. Invest. 101, 604–612 (1998).
R.D. Levere, P. Martasek, B. Escalante, M.L. Schwartzmannn, and N.G. Abranam, Effect of heme arginate administration on blood pressure in spontaneously hypertensive rats, J. Clin. Invest. 86, 213–219(1990).
R.A. Johnson, M. Lavesa, D. Askari, N.G. Abraham, and A. Nasjletti, A heme oxygenase product, presumably carbon monoxide, mediates a vasodepressor function in rats, Hypertension. 25, 166–169 (1995).
M. Maines and D. Trakshel, Differential regulation of heme oxygenase isozymes by Sn- and Zn-protoporphyrins: possible relevance to suppression of hyperbilirubinemia, Biochem. Biophys. Acta. 1131, 166–174 (1992).
N.L. Kanagy, Increased vascular responsiveness to alpha 2-adrenergic stimulation during NOS inhibition-induced hyperension, Am. J. Physiol. 273, H2756–H2764 (1997).
E. Nisoli, E. Clementi, C. Tonello, C. Sciorati, L. Briscini, and M.O. Carruba, Effects of nitric oxide on proliferation and differentiation of rat brown adipocytes in primary cultures, Br. J. Pharmacol. 125, 888–894 (1998).
Y. Shinoda, M. Suematsu, Y. Wakabayashi, T. Suzuki, N. Goda, S. Saito, T. Yamaguchi, and Y. Ishimura, Carbon monoxoide as a regulator of bile canalicular contrctility in cultured rat hepatocytes, Hepatology. 28, 286–295 (1998).
D. Luo and S.R. Vincent, Metalloporphyrins inhibit nitric oxide-dependent cGMP frmation in vivo, Eur. J. Pharmacol. 267, 253–262 (1994).
M.K. Meffert, J.E. Haley, E.M. Schuman, H. Schulman, D.V. Madison, Inhibition of Hippocampal heme oxygenase, nitric oxide synthese, and long-term potentiation by metalloporphyrins, Neuron. 13, 1225–1233 (1994).
T. Naruko, K. Ueda, K. Haze, A.C. van der Wal, C.M. van der Loos, K. Tanzawa, and A.E. Becker, Endothelin and endothelin-converting enzyme expression at the site of percutaneus transluminal coronary angioplasty in humans, Circulation. 96, 1–348 (1997).
H. Rakugi, H.J. Jacob, J.E. Krieger, J.R. Ingelfinger, and R.E. Pratt, Vascular injury induces angiotensinogen gene expression in the media and neointima, Circulation. 87, 283–290 (1993).
R. Zakhary, S.P. Gaine, J.L. Dinerman, M. Ruat, N.A. Flavahaan, and S.H. Snyder, Heme oxygenase 2: Endothelial and neuronal localization and role in endothelium-dependent relaxation, Proc. Natl. Acad. Sci. USA. 93, 795–798 (1996).
G.A. Ferns, L. Forster, L.A. Stewart, M. Konneh, Z.J. Nouroos, and E.E. Anggard, Probucol inhibits neointimal thickening and macrophage accumulation after balloon injury in the cholesterolfed rabbit, Proc. Natl. Acad. Sci. USA. 89, 11312–11316 (1992).
C.T. Wagner, W. Durante, N. Christodoullides, J.D. Heliums, and A.I. Schafer, Hemodynamic forces induced the expression of heme oxygenase in cultured vascular smooth muscle cells, J. Clin. Invest. 100, 589–596 (1997).
S.M. Schwartz, D. deBlois, and E.R. O’Brien, The intima:soil for atherosclerosis and restenosis, Circ. Res. 77, 445–465 (1995).
L.J. Wang, T.S. Lee, F.Y. Lee, R.C. Pai, and L.Y. Chau, Expression of heme oxygenase-1 in atherosclerotic lesions, Am. J. Pathol. 152, 711–720 (1998).
F. Coceani, L. Kelsey, and E. Seidlitz, Carbon monoxide-induced relaxation of the ductus arteriosus in the lamb: evidence against the prime role of guanylyl cyclase, Br. J. Pharmacol 118,1689–1696 (1996).
F. Coceani, C.A. Breen, J.G. Lees, J.R. Falck, and P.M. Olley, Further evidence implicating a cytochrome P 450-mediated reaction in the contractile tension of lamb ductus arteriosus, Cir. Res. 62, 471–477 (1988).
H. Lin and J.J. McGrath, Carbon monoxide effects on calcium levels in vascular smooth muscle, Life Sci. 43, 1813–1816 (1988).
H. Lin and J.J. McGrath, Is carbon monoxide a calcium blocking agent? I. Effect of carbon monoxide on mechanical tension in isolated thoracic aorta, Fed. Proc. 2, A 372 (1988).
R. Wang, Z.Z. Wang, and L. Wu, Carbon monoxide-induced vasorelaxation and underlying mechanisms, Br. J. Phramacol. 121, 927–934 (1997).
Author information
Authors and Affiliations
Corresponding author
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2002 Springer Science+Business Media New York
About this chapter
Cite this chapter
Morita, T., Togane, Y., Suematsu, M., Yamazaki, Ji., Katayama, S. (2002). Endogenous Carbon Monoxide has Protective Roles in Neointimal Development Elicited by Arterial Injury. In: Abraham, N.G. (eds) Heme Oxygenase in Biology and Medicine. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0741-3_4
Download citation
DOI: https://doi.org/10.1007/978-1-4615-0741-3_4
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4613-5219-8
Online ISBN: 978-1-4615-0741-3
eBook Packages: Springer Book Archive