title: Role of heme oxygenase in preserving vascular bioactive NO.
abstract: Beyond its vasodilator role, vascular nitric oxide (NO), which is synthesized by endothelial NO synthase (eNOS) via its activation, has been shown to play a number of other beneficial roles in the vascular system; it inhibits proliferation of vascular smooth muscle cells, prevents platelet aggregation, and regulates endothelial apoptosis. Such beneficial roles have been shown to be implicated in the regulation of endothelial functions. A loss of NO bioavailability that may result either from decreased eNOS expression and activity or from increased NO degradation is associated with endothelial dysfunction, a key factor in the development of vascular diseases. Heme oxygenase-1 (HO-1), an inducible enzyme, catalyzes the oxidative degradation of heme to free iron, carbon monoxide, and biliverdin, the latter being subsequently converted into bilirubin. In the vascular system, HO-1 and heme degradation products perform important physiological functions, which are ultimately linked to the protection of vascular cells. Studies have shown that HO-1 and heme degradation products exert vasodilatory, antioxidant, anti-inflammatory, antiproliferative and anti-apoptotic effects on vascular cells. Interestingly, these effects of HO-1 and its by-products are similar, at least in part, to those of eNOS-derived NO; this similarity may prompt investigators to study a possible relationship between eNOS-derived NO and HO-1 pathways. Many studies have been reported, and accumulating evidence suggests that HO-1 and heme degradation products can improve vascular function, at least in part, by compensating for the loss of NO bioavailability. This paper will provide the possible pathway explaining how HO-1 and heme degradation products can preserve vascular NO.
authors: Department of Microbiology and Immunology, Wonkwang University School of Medicine, Iksan 570-749, Republic of Korea.
authors: Hyun-Ock
authors: HO
authors: Pae
authors: Yong
authors: Y
authors: Son
authors: Nam-Ho
authors: NH
authors: Kim
authors: Hee Jong
authors: HJ
authors: Jeong
authors: Ki Churl
authors: KC
authors: Chang
authors: Hun-Taeg
authors: HT
authors: Chung
mesh_terms: D000818:Animals; D051547:Heme Oxygenase-1 / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D011494:Protein Kinases / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D014157:Transcription Factors; D009569:Nitric Oxide; D052250:Nitric Oxide Synthase Type III; D051547:Heme Oxygenase-1; D011494:Protein Kinases