期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 276, 期 31, 页码 29251-29256出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M102124200
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资金
- NCI NIH HHS [P01 CA066081, CA66081] Funding Source: Medline
- NHLBI NIH HHS [K08 HL003669-05, R01 HL51469, R01 HL051469, K08 HL003669-03, K08 HL003669-04, HL62984, HL49264, P01 HL062984] Funding Source: Medline
Non-phagocytic NAD(P)H oxidases have been implicated as major sources of reactive oxygen species in blood vessels. These oxidases can be activated by cytokines, thereby generating O-2(radical anion), which is subsequently converted to H2O2 and other oxidant species. The oxidants, in turn, act as important second messengers in cell signaling cascades. We hypothesized that reactive oxygen species, themselves, can activate the non-phagocytic NAD(P)H oxidases in vascular cells to induce oxidant production and, consequently, cellular injury. The current report demonstrates that exogenous exposure of non-phagocytic cell types of vascular origin (smooth muscle cells and fibroblasts) to H2O2 activates these cell types to produce O-2* via an NAD(P)H oxidase. The ensuing endogenous production of O-2* contributes significantly to vascular cell injury following exposure to H2O2. These results suggest the existence of a feed-forward mechanism, whereby reactive oxygen species such as H2O2 can activate NAD(P)H oxidases in non-phagocytic cells to produce additional oxidant species, thereby amplifying the vascular injury process. Moreover, these findings implicate the non-phagocytic NAD(P)H oxidase as a novel therapeutic target for the amelioration of the biological effects of chronic oxidant stress.
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