11/20/2023 0 Comments Al carbonMKK3 and MKK6 regulation of gene expression is mediated by the p38 MAP kinase signal transduction pathway. Raingeaud, J., Whitmarsh, A.J., Barrett, T., Derijard, B. Independent human MAP kinase signal transduction pathways defined by MEK and MKK isoforms. Dynamics of carbon monoxide binding with neuronal nitric oxide synthase. Tetreau, C., Tourbez, M., Gorren, A., Mayer, B. Carbon monoxide, a putative neural messenger. Verma, A., Hirsch, D.J., Glatt, C.E., Ronnett, G.V. Smooth muscle cell-derived carbon monoxide is a regulator of vascular cGMP. Nitric oxide inhibits inflammatory cytokine production by human alveolar macrophages. Pro-inflammatory cytokines and environmental stress cause p38 mitogen-activated protein kinase activation by dual phosphorylation on tyrosine and threonine. Raingeaud, J., Gupta, S., Han, J., Ulevitch, R.J. A MAP kinase targeted by endotoxin and hyperosmolarity in mammalian cells. Activation of c-Jun N-terminal kinase in bacterial lipopolysaccharide-stimulated macrophages. Toll-like receptor-4 mediates lipopolysaccharide-induced signal transduction. Toll-like receptor-2 mediates lipopolysaccharide-induced cellular signaling. Interleukin-10 protects mice from lethal endotoxemia. Lipopolysaccharide-induced production of tumor necrosis factor and interleukin-1 is differentially regulated at the receptor level: the role of CD14-dependent and CD14-independent pathways. Control of cachectin (tumor necrosis factor) synthesis: mechanisms of endotoxin resistance. Advances in the understanding of pathogenesis, cardiovascular dysfunction and therapy. Parillo, J.E., Parker, M.M., Natanson, A.F., Suffredini, R.L. Exogenous administration of heme oxygenase-1 by gene transfer provides protection against hyperoxia-induced lung injury. Overexpression of heme oxygenase-1 in human pulmonary epithelial cells results in cell growth arrest and increased resistance to hyperoxia. Hemoglobin provides protection against lethal endotoxemia in rats: the role of heme oxygenase-1. Oxidative stress causes enhanced endothelial cell injury in human heme oxygenase-1 deficiency. Yachie, A., Niida, Y., Wada, T., Igarashi, N. Reduced stress defense in heme oxygenase deficient cells. Induction of heme oxygenase is a rapid, protective response in rhabdomyolysis in the rat. The enzymatic conversion of heme to bilirubin by microsomal heme oxygenase. These data indicate the possibility that carbon monoxide may have an important protective function in inflammatory disease states and thus has potential therapeutic uses. Carbon monoxide mediated these anti-inflammatory effects not through a guanylyl cyclase–cGMP or nitric oxide pathway, but instead through a pathway involving the mitogen-activated protein kinases. Both in vivo and in vitro, carbon monoxide at low concentrations differentially and selectively inhibited the expression of lipopolysaccharide-induced pro-inflammatory cytokines tumor necrosis factor-α, interleukin-1β, and macrophage inflammatory protein-1β and increased the lipopolysaccharide-induced expression of the anti-inflammatory cytokine interleukin-10. We demonstrate here that carbon monoxide, a by-product of heme catabolism by heme oxygenase, mediates potent anti-inflammatory effects. The anti-inflammatory properties of heme oxygenase-1 may serve as a basis for this cytoprotection. The stress-inducible protein heme oxygenase-1 provides protection against oxidative stress.
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