Carbon monoxide from heme catabolism protects against hepatobiliary dysfunction in endotoxin-treated rat liver

Leydig cell–derived heme oxygenase-1 regulates apoptosis of premeiotic germ cells in response to stress

“…Ad4BP is a transcriptional factor constitutively expressed in nuclei of steroidogenic cells and serves as a reliable marker to identify Leydig cells and Sertoli cells in testis (13). Microtopographic distribution of HO-derived CO generation was examined immunohistochemically by an anti-bilirubin-IXα mAb 24G7 (14,15). Contents of microsomal P450 monooxygenases in testicular tissues were determined as described previously (16).…”

Cystathionine β-synthase as a carbon monoxide-sensitive regulator of bile excretion

“…The CO-overproducing livers down-regulated H 2 S to stimulate HCO 3 ؊ -dependent choleresis: these responses were attenuated by blocking HO C arbon monoxide (CO) is generated from inducible heme oxygenase 1 (HO-1) and constitutive heme oxygenase 2 (HO-2), respectively, and has the ability to regulate neurovascular functions, 1,2 apoptotic responses, 3,4 and metabolism of xenobiotics and toxicants. 5,6 This gas is overproduced through increased delivery of heme as a substrate and the HO-1 induction on exposure to stressors such as hypoxia and oxidative stress. Mechanisms by which CO regulates cell functions appear to involve an activation of soluble guanylate cyclase (sGC), the enzyme that allows the gas to bind to the prosthetic heme to synthesize cyclic guanosine monophosphate as a second messenger.…”

“…5,6 This gas is overproduced through increased delivery of heme as a substrate and the HO-1 induction on exposure to stressors such as hypoxia and oxidative stress. Mechanisms by which CO regulates cell functions appear to involve an activation of soluble guanylate cyclase (sGC), the enzyme that allows the gas to bind to the prosthetic heme to synthesize cyclic guanosine monophosphate as a second messenger.…”

“…5,6,12 However, ferrous heme of these enzymes is not only sensitive to CO but to NO. In this context, whether mechanisms by which CO regulates cell and organ functions is not shared by those for NO has not fully been studied yet.…”

rAAV-mediated stable expression of heme oxygenase-1 in stellate cells: A new approach to attenuate liver fibrosis in rats

“…12 Although expression of HO-1 in the liver is restricted to a subpopulation of Kupffer cells, 13 the gene is inducible in both parenchymal and particularly nonparenchymal liver cells under stress conditions. 14 Protective effects of enhanced HO enzymatic activity-probably through its products-have been reported in various disease-related models, [15][16][17][18] but the functional role as well as the therapeutic potential of HO-1 in liver fibrogenesis is still unknown. Importantly, no evidence is available on whether HO-1 can be targeted for the treatment of liver fibrosis.…”