Abstract
Heme oxygenase (HO) is the rate-limiting enzyme to catalyze the heme degradation, leading to the generation of biliverdin, which is subsequently converted to antioxidant bilirubin by biliverdin reductase,1,2 free iron, and carbon monoxide (CO). Three HO isozymes derived from distinct genes were identified.3 Among them, HO-1 is a stress-responsive protein and can be induced by a variety of oxidative-inducing agents, including heme, heavy metals, UV radiation, cytokines, and endotoxin.4,5 Recently, numerous in vitro and in vivo studies have demonstrated that the induction of HO-1 represents an important cellular protective mechanism against oxidative injury.4,5 In addition to the antioxidant effect of bilirubin,6–8 increasing interest has been drawn on the potential effects of CO. It has been shown that CO shares similar properties with nitric oxide (NO) to act as a putative neural transmitter in central nervous system and a potent vasodilator to regulate the vascular tone through the activation of soluble guanylate-cyclase-cGMP pathway.9–11 Both gases also exert potent anti-proliferative effect on vascular smooth muscle cells (VSMCs).12–15 Very recently, there are studies demonstrating that low concentration of CO provides protection against hyperoxic lung injury in animal16 and apoptotic death in fibroblasts and endothelial cells induced by TNF-α.17,18 Furthermore, a study on macrophages has shown that CO exhibits anti-inflammatory effect through a pathway involving the mitogen-activated protein kinases.19 It is apparent that CO mediates some of the beneficial effects of HO-1 induction under certain circumstances.
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References
M.D. Maines, Heme oxygenase: function, multiplicity, regulatory mechanisms and clinical applications,FASEB J.2(10), 2557–2568 (1988).
P. Ponka, Cell biology of heme,Am. J. Med Sci.318(4), 241–256 (1999).
M.D. Maines, The oxygenase system: A regulator of second messenger gases,Annu. Rev. Pharmacol Toxicol 37, 517–554 (1997).
J.L. Platt and K.A. Nath, Heme oxygenase: protective gene or Trojan horse,Nature Med.4(12), 1364–1365(1998).
L.E. Otterbein and A.M.K. Choi, Heme oxygenase: colors of defense against cellular stress,Am. J. Physiol Lung Cell Mol. Physiol 279(6), L1029–L1037 (2000).
R. Stocker, Y. Yamamoto, A.F. McDonagh, A.N. Glazer, and B.N. Ames, Bilirubin is an antioxidant of possible physiological importance,Science 235(4792), 1043–1046 (1987).
S.F Llesuy, S.F., and M.L. Tomaro, Heme oxygenase and oxidative stress: evidence of involvement of bilirubin as physiological protector against oxidative damage,Biochim. Biophys. Acta 1223(1), 9–14 (1994).
R. Stocker, Induction of haem oxygenase as a defense against oxidative stress,Free Radical Res. Commun.9(2), 101–112 (1990).
H.H. Schmidt, NO, CO, and HO endogenous soluble guanylyl cyclase-activating factors,FEBS Lett.307(1), 102–107 (1992).
A. Verma, D.J. Hirsch, C.E. Glatt, G.V. Ronnett, and S.H. Snyder, Carbon monoxide: a putative neural messenger,Science 259(5093), 381–384 (1993).
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(5), 1475–1479 (1995).
D.M. Lloyd-Jones and K.D. Bloch, The vascular biology of nitric oxide and its role in atherosclerosis,Annu. Rev. Med.47, 365–375 (1996).
M. Kibbe, T. Billiar, and E. Tzeng, Inducible nitric oxide synthase and vascular injury,Cardiovas. Res.43(3), 650–657 (1999).
Y. Togane, T. Morita, M. Suematsu, Y. Ishimura, J.I. Yamazaki, and S. Katayama, Protective roles of endogenous carbon monoxide in neointimal development elicited by arterial injury,Am. J. Physiol. Heart Circ. Physiol.278(2), H623–H632 (2000).
T. Morita, S.A. Mitsialis, H. Koike, Y. Liu, and S. Kourembanas, Carbon monoxide controls the proliferation of hypoxic vascular smooth muscle cells.J. Biol. Chem.272(52), 32804–32809 (1997).
L.E. Otterbein, L.L. Mantell, and A.M.K. Choi, Carbon monoxide provides protection against hyperoxic lung injury,Am. J. Physiol.276(4 Pt1), L688–L694 (1999).
I. Petrache, L.E. Otterbein, J. Alam, G.W. Wiegand, and A.M.K. Choi, Heme oxygenase-1 inhibits TNF-α-induced apoptosis in cultured fibroblasts,Am. J. Physiol. Lung Cell Mol. Physiol.278(2), L312–L319(2000).
S. Brouard, L.E. Otterbein, J. Anrather, E. Tobiasch, F.H. Bach, A.M.K. Choi, and M.P. Soares, Carbon monoxide generated by heme oxygenase-1 suppresses endothelial cell apoptosis,J. Exp. Med.192(7), 1015–1025 (2000).
L.E. Otterbein, F.H. Bach, J. Alam, M. Soares, H.T. Lu, M. Wysk, R.J. Davis, R.A. Flavell, and A.M.K. Choi, Carbon monoxide has anti-inflammatory effects involving the mitogen-activated protein kinase pathway,Nature Med.6(4), 422–428 (2000).
A. Ernst and J.D. Zibrak, Carbon monoxide poisoning,N. Engl. J. Med.339(22), 1603–1608 (1998).
J.S. Stamler and C.A. Piantadosi, O=O NO: It’s CO.,J. Clin. Invest.97(10), 2260–2267 (1996).
M.O. Hengartner, The biochemistry of apoptosis,Nature 407(6805), 770–776 (2000).
PA. Dennery, K.J. Sridhar, C.S. Lee, H.E. Wong, V. Shokoohi, P.A. Rodgers, and D.R. Spitz, Heme oxygenase-mediated resistance to oxygen toxicity in Hamster fibroblasts,J. Biol. Chem.272(23), 14937–14942 (1997).
D.M. Suttner and P.A. Dennery, Reversal of HO-1 related cytoprotection with increased expression is due to reactive iron,FASEB J.13(13), 1800–1809 (1999).
K. Fisher-Dzoga, R.M. Jones, D. Vesselinbovitch, and R.W. Wissler, Ultrastructural and immuno-histochemical studies of primary cultures of aortic medial cells,Exp. Mol. Pathol.18(2), 162–176 (1973).
J. Zhang and C.A. Piantadosi, Mitochondrial oxidative stress after carbon monoxide hypoxia in the rat brain,J. Clin. Invest.90(4), 1193–1199 (1992).
H. Ischizopoulos, M.F. Beers, S.T. Ohnishi, D. Fisher, S.E. Garner, and S.R. Thorn, Nitric oxide production and perivascular tyrosine nitration in brain after carbon monoxide poisoning in the rat,J. Clin. Invest.97(10), 2260–2267 (1996).
S.R. Thorn, S.T. Ohnishi, D. Fisher, Y.A. Xu, and H. Ischiropoulos, Pulmonary vascular stress from carbon monoxide,Toxicol. Appl. Pharmacol.154(1), 12–19 (1999).
S.R. Thorn, D. Fisher, Y.A. Xu, S. Garner, and H. Ischiropoulos, Role of nitric oxide-derived oxidants in vascular injury from carbon monoxide in the rat,Am. J. Physiol. Heart Circ. Physiol.276(3 Pt2), H984–H992 (1999).
V. Turcanu, M. Dhouib, J-L. Gendrault, and P. Poindron, Carbon monoxide induces murine thymocyte apoptosis by a free-radical mediated mechanism,Cell Biol & Toxicol.14(1), 47–54 (1998).
S.R. Thorn, D. Fisher, Y.A. Xu, K. Notarfrancesco, and H. Ischiropoulos, Adaptive responses and apoptosis in endothelial cells exposed to carbon monoxide,Proc. Natl. Acad. Sci. USA 97(3), 1305–1310(2000).
M. Iwashina, M. Shichiri, F. Marumo, and Y. Hirata, Transfection of inducible nitric oxide synthase gene causes apoptosis in vascular smooth muscle cells,Circulation 98(12), 1212–1218 (1998).
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(3), 711–720 (1998).
T. Aizawa, N. Ishizaka, J. Taguchi, S. Kimura, K. Kurokawa, and M. Ohno, Balloon injury does not induce heme oxygenase-1 expression, but a dministration of hemin inhibits neointimal formation in balloon-injured rat carotid artery,Biochem. Biophys. Res. Commun.261(2), 302–307 (1999).
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Juan, SH., Chau, LY. (2002). Induction of Apoptosis in Vascular Smooth Muscle Cells by Heme Oxygenase-1-Derived Carbon Monoxide. In: Abraham, N.G. (eds) Heme Oxygenase in Biology and Medicine. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0741-3_40
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DOI: https://doi.org/10.1007/978-1-4615-0741-3_40
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