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Pulmonary artery endothelial cells bovine

Phenol, 1,1,2- trichloroethane, cyanide, lindane, pentachlorophenate (PCP) Impedance Bovine pulmonary artery endothelial cells, bovine lung microvessel endothelial cells Adsorption n.r. n.r. 173... [Pg.301]

MDCK (Madin-Darby canine kidney) cells are derived from distal tubules, whereas LLC-PKi are from proximal tubes. b BMEC (brain microvessel endothelial cells) are isolated from capillaries. BPAEC (bovine pulmonary artery endothelial cells), BAEC (bovine aortic endothelial cells), and HUVEC (human umbilical vein endothelial cells) are large vessel endothelia. [Pg.241]

BPAEC, bovine pulmonary artery endothelial cells... [Pg.29]

High antioxidative activity carvedilol has been shown in isolated rat heart mitochondria [297] and in the protection against myocardial injury in postischemic rat hearts [281]. Carvedilol also preserved tissue GSL content and diminished peroxynitrite-induced tissue injury in hypercholesterolemic rabbits [298]. Habon et al. [299] showed that carvedilol significantly decreased the ischemia-reperfusion-stimulated free radical formation and lipid peroxidation in rat hearts. Very small I50 values have been obtained for the metabolite of carvedilol SB 211475 in the iron-ascorbate-initiated lipid peroxidation of brain homogenate (0.28 pmol D1), mouse macrophage-stimulated LDL oxidation (0.043 pmol I 1), the hydroxyl-initiated lipid peroxidation of bovine pulmonary artery endothelial cells (0.15 pmol U1), the cell damage measured by LDL release (0.16 pmol l-1), and the promotion of cell survival (0.13 pmol l-1) [300]. SB 211475 also inhibited superoxide production by PMA-stimulated human neutrophils. [Pg.885]

Later on, the importance of xanthine oxidase as the producer of reoxygenation injury was questioned at least in the cells with low or no xanthine oxidase activity. Thus, it has been shown that human and rabbit hearts, which possess extremely low xanthine oxidase activity, nonetheless, develop myocardial infractions and ischemia-reperfusion injury [9], However, recent studies supported the importance of the xanthine oxidase-catalyzed oxygen radical generation. It has been showed that xanthine oxidase is partly responsible for reoxygenation injury in bovine pulmonary artery endothelial cells [10], human umbilical vein and lymphoblastic leukemia cells [11], and cerebral endothelial cells [12], Zwang et al. [11] concluded that xanthine dehydrogenase may catalyze superoxide formation without conversion to xanthine oxidase using NADH instead of xanthine as a substrate. [Pg.917]

The sample used for a demonstration of broadband TPF imaging with compressed PCF supercontinuum in Figure 7.17 was a commercially available test slide (Invitrogen FluoCells , prepard slide 1, containing labeled bovine pulmonary artery endothelial cells). The conventional optical phase-contrast microscopy image... [Pg.191]

S. L. Lee and B. L Rmburg. Serotonin uptake by bovine pulmonary artery endothelial cells in culture. ] Charatterization. Am. J. PkysiaL 2JftC7fi]-C765 (1986)... [Pg.33]

Hsieh, T.C., Juan, G.L., Darzynkiewicz, Z., and Wu, J.M., Resveratrol increases nitric oxide synthase, induces accumulation of p53 and p21 wafi/cipi suppresses cultured bovine pulmonary artery endothelial cell proliferation by perturbing progression through S and Gj, Cancer Res., 59, 2596, 1999. [Pg.159]

S-allyl cysteine (SAC), was found to protect bovine pulmonary artery endothelial cells from oxidant injury induced by hydrogen peroxide (H2O2). Also, SAC may act via antioxidant mechanisms to block NF-kappa B activation in Jurkat cells in which it consistently exhibited a dose-dependent inhibition of NF-kappa B activation induced by both TNF-alpha and H2O2. Supershift with specific antibodies to NF-kappa B subunits confirmed that the inducible retarded bands observed in the... [Pg.471]

Evidence suggests that resveratrol may protect against atherosclerosis by enhancing endothelium integrity through the inhibition of protein kinase C (PKC)-mediated signaling [62]. However, resveratrol was also shown to inhibit protein kinase D, a member of the PKC family, but did not affect other PKC isoforms [63, 64]. Furthermore, effects observed in bovine pulmonary artery endothelial cells subjected to stimulated arterial shear stress were also shown to be unrelated to PKC [65]. [Pg.236]

Bruder JL, Hsieh Tc T, Lerea KM, Olson SC, Wu JM. Induced cytoskeletal changes in bovine pulmonary artery endothelial cells by resveratrol and the accompanying modified responses to arterial shear stress. BMC Cell Biol 2001 2 1. [Pg.248]

Others have demonstrated that hyperoxia altered cultured bovine pulmonary arterial endothelial cells in such a way that they released more 6-keto-PGFjjj and LTB4 upon stimulation with Ca " ionophore. Again it is unclear whether the ultrastructural changes of the endothelial cells (bleb formation, decreased membrane barrier) facilitates influx and LTB4 synthesis or... [Pg.79]

Phenylarsine oxide, an inhibitor of tyrosine phosphatase, caused a dose-dependent decrease in eNOS activity in total membrane and in purified eNOS fractions from porcine pulmonary artery endothelial cells, even though the latter had no detectable tyrosine phosphatase activity (Su and Block 2000). Phenylarsine oxide also caused a decrease in sulphydryl content and eNOS activity in purified bovine eNOS. The reduction in eNOS sulphydryl content and the inhibitory effect of phenylarsine oxide on eNOS activity were prevented by dithio-threitol, a disulphide-reducing agent. [Pg.409]

Lipopolysaccharide (0.5 /tg/ml) and tumour necrosis factor-a (0.5 ng/ml) treatment increased l-arginine metabolism to both NO and urea in bovine pulmonary arterial endothelial cell cultures and resulted in increased levels of cationic amino acid transporter-2 mRNA (Nelin et al. 2001). [Pg.417]

FIGURE 35.1 Typical trajectory of a bovine pulmonary artery endothelial cell migrating in a uniform environment. Symbols represent the position of the centroid of the same cell recorded at 30 min intervals (top panel) and 3 h intervals (bottom panel). When the observation interval is short (top panel), the cell clearly exhibits persistence in movement direction. If a long observation interval (bottom panel) is chosen, however, the movement of the same cell appears to be a random walk with frequent direction changes. (Adapted from Lee, Y., Mcintire, L.V., and Zygourakis, K., Biochem. Cell Biol, 1995, 73 461 72. With permission.)... [Pg.555]

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. [Pg.164]

Spr RG. DNA strand break formation following exposure of bovine pulmonary artery and aortic endothelial cells to reactive oxygen products. Am J Respir Cell Mol Biol 1991 4 4-10. [Pg.196]


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See also in sourсe #XX -- [ Pg.79 ]




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