Endothelial cells injury

Grosso, M.A., Brown, J.M., Viders, D.E., Mulvin, D.W., Banerjee, A., Velasco, S.E. and Repine, J.E. (1989). Xanthine oxidase-derived oxygen radicals induce pulmonary edema via direct endothelial cell injury. J. Suig. Res. 46, 355-360. 

Beckman, J.S., Beckman, T.W., Chen, J., Marshall, P.A. and Freeman, B.A. (1990). Apparent hydroxyl radical formation by peroxynitrite implications for endothelial cell injury from nitric oxide and superoxide anion. Proc. Natl Acad. Sci. USA 87, 1620-1624. 

Hernandez-Montes E, Pollard SE, Vauzour D, Jofre-Montseny L, Rota C, Rimbach G, Weinberg PD and Spencer JPE. 2006. Activation of glutathione peroxidase via Nrfl mediates genistein s protection against oxidative endothelial cell injury. Biochem Biophys Res Commun 346(3) 851—859. 

Glutathione peroxidase is a selenium-dependent enzyme, which rapidly detoxifies hydrogen peroxide and various hydroperoxides. Suttorp et al. [67] showed that the impairment of glutathione cycle resulted in an increase in the injury of pulmonary artery endothelial cells. Glutathione cycle protected against endothelial cell injury induced by 15-HPETE, an arachi-donate metabolite produced by 15-lipoxygenase-catalyzed oxidation [68]. 

HO-1 is controlled at the level of transcription by oxidative stress and several inducers such as porphyrins, metals, and progesterone (8). The absence of HO-1 is associated with severe growth retardation, anemia, and enhanced endothelial cell injury 156, 157). In addition, HO-1 has been implicated in protection against transplant rejection 158, 159). HO-2 is constitutively expressed, and its presence in brain and the noted similar effects of CO and NO has led to the proposal that CO-generated by HO-2 is involved in signaling processes 8, 160-162). 

Hollinger MA. 1982. Biochemical evidence for pulmonary endothelial cell injury after carbon tetrachloride administration in mice. J Pharmacol Exp Therap 222 641-4. 

Murota, S.I., Morita, I., and Suda, N. 1990. The control of vascular endothelial cell injury. Ann NY... 

Vascular intervention results in cellular injury and the release of several mediators of thrombotic and inflammatory processes. Endothelial cell injury results in luminal thrombosis, inflammatory cell infiltration, cellular proliferation, and... 

I Wall RT et al. Homocysteine-induced endothelial cell injury in vitro a model for the study of vascular injury. Thromb Res 1980 18(1-2) I 13-121. 

Arditi, M., Zhou, J., Dorio, R., Rong, G.W., Goyert, S.M., Kim, K.S. Endotoxin-mediated endothelial cell injury and activation Role of soluble CD14. Infect Immun 61 (1993) 3149-3156. 

Nakatani K, Takeshita S. Vascular endothelial cell injury by activated neutrophil and treatment for the injury. Surg Trauma Immunol Respon 1999 8 112-114. 

Nakatani K, Takeshita S, Tsujimoto H, Kawamura Y, Sekine I. Inhibitory effect of serine protease inhibitors on neutrophil-mediated endothelial cell injury. J Leukoc Biol 2001 ... 

Sevanian, A., Hodis, H.N., Hwang, J., McLeod, L.L., Peterson, H. 1995. Characterization of endothelial cell injury by cholesterol oxidation products found in oxidized LDL. J. Lipid Res. 36, 1971-1986. 

Atkins, K.B., Lodhi, I.J., Hurley, L.L., Hinshaw, D.B. (2000). A-acetylcysteine and endothelial cell injury by sulfur mustard. J. Appl. Toxicol. 20 (Suppl. 1) SI25-8. 

As the knowledge of the pathogenesis of atherosclerosis rapidly increases, it appears that an active vascular endothelium, smooth muscle cells, and blood-borne cells such as monocytes and macrophages all play active roles in the atherosclerotic disease process. Risk factors, such as elevated plasma levels of certain lipids, prooxidants, and cytokines, may contribute to the chronic activation/stimulation as well as to the damage of the endothelium and other vascular tissues (160). There is evidence that supports the hypothesis that it is not only pure cholesterol and saturated fats but rather oxidation products of cholesterol and unsaturated fats (and possibly certain pure unsaturated fats) that are atherogenic, possibly by causing endothelial cell injury/dysfiinction. Lipid-mediated endothelial cell dysfunction may lead to adhesion of monocytes, increased permeability of the endothelium to macromolecules, i.e., a decrease in endothelial barrier function, and disturbances in growth control of the vessel wall. 

There is experimental evidence that suggests that some oxysterols, but not pure cholesterol, are the prime cause of atherosclerotic lesion formation (162). Upon cholesterol feeding, a strong relationship was seen between plasma oxysterols and aortic wall oxysterols. One may speculate that the deposition of pure lipids, such as cholesterol and its esters, may be merely a secondary process in response to oxysterol-induced endothelial cell injury. Cell injury/dysfunction and the subsequent disruption of endothelial barrier function by oxysterols (163, 164) could initiate the early events in atherosclerosis. Such injury could allow increased uptake... 

Cutaia M, Bullard SR, Rudio K, Rounds S. Characteristics of amphotericin B-induced endothelial cell injury. J Lab Clin Med... 

There are several lines of evidence demonshahng that CSA causes endothelial cell injury. CSA has a direct cytotoxic effect on cultured endothelial cells and inhibits human umbilical endothelial cell proliferahon [74,75]. CSA increases the plasma level of endothelial damage markers, such as Von Willebrand factor, endothelin tissue factor pathway inhibitor, P-selectin and thrombin-antithrombin complexes in renal and heart transplant patients [76-79]. Similarly, the release of Von... 

Zoja C, Furci L, Ghilardi E, Zilio P, Benigni A, Remuzzi G. Cyclosporin-induced endothelial cell injury. Lab Invest 1986 55 455-462. 

Rafj-Janajreh AQ, Chen D, Schmits R, MakTW, Grayson RL, Sponenberg DP, Nagarkatti M, Nagarkatti PS Evidence forthe involvement ofCD44 in endothelial cell injury and induction of vascular leak syndrome by IL-2, J Immunol 1999,163 1619-1627... 

Lead-induced hyperuricemia may contribute to chronic lead nephropathy. Uric acid per se induces endothelial cell injury, renal microvascular disease, and hypertension, at least in part mediated by oxidative stress [38]. Independent of uric acid, reactive oxygen species induced by lead have been imphcated in endothelial cell injury, increased vascular reactivity, and the production of hypertension in humans and experimental animals [39]. 

Meyrick, L.C., Hoffman, L.H. and Brigham, K.L. (1984). Chemotaxis of granulocytes across bovine pulmonary artery intimal explants without endothelial cell injury. Tissue Cell 16, 1-16. 

Activated neutrophils and platelets adhere to the pulmonary capillary endothelium, initiating multiple inflammatory cascades with a release a variety of toxic substances. There is diffuse pulmonary endothelial cell injury, increased capillary permeability, and alveolar epithelial cell injury. Consequently, interstitial pulmonary edema occurs and gradually progresses to alveolar flooding and collapse. The end result is loss of functional alveolar volume, impaired pulmonary compliance, and profound hypoxemia. ... 

Yachie, A., Niida, Y., Wada, T., Igarashi, N., Kaneda, H., Toma, T., Ohta, K., Kasa-hara, Y. and Koizumi,. Oxidative stress causes enhanced endothelial cell injury in human heme oxygenase-1 deficiency. Journal of Clinical Investigation 103 129-135 1999. 

Inhibition of Neutrophil-Mediated Human Aortic Endothelial Cell Injury by Superoxide Dismutase Mimics... 

In the neutrophil-mediated, endothelial cell injury assay, the SOD mimics protected against the injury to a greater extent than the SOD enzyme did under conditions where the same amounts of SOD activity of the SOD mimics and of the enzyme were used. These results are consistent with the SOD mimics gaining access to the intracellular space of the cells, thereby catalyzing the dismutation of intracellular superoxide, which the SOD enzyme cannot gain access to. Therefore, the lipophilicities of the SOD mimics are expected to be critical in obtaining optimal protection of the intracellular space against superoxide-mediated cytotoxicity. 

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