Pulmonary artery endothelial cells

Phon, S.H., Gannon, D.E., Varan, J., Ryan, V.S. and Ward, P.A. (1989). Xanthine oxidase activity in rat pulmonary artery endothelial cells and its alteration by activated neutrophils. Am. J. Path. 134, 1201-1211. 

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. 

BPAEC, bovine pulmonary artery endothelial cells... 

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. 

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]. 

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. 

Gupta, M. P., Evanoff, V., and Hart, C. M., 1997, Nitric oxide attenuates hydrogen peroxide-mediated injury to pordne pulmonary artery endothelial cells, Am. J. Physiol. 272 LI 133-1141. 

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... 

Ullmer C, Boddeke HG, Schmuck K, Lubbert H. 5-HT2B receptor-mediated calcium release from ryanodine-sensitive intracellular stores in human pulmonary artery endothelial cells. Br J Pharmacol 1996 117 1081-1088. 

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

Figure 2. Cultured pulmonary artery endothelial cells stained for tubulin (red), actin (green) and DNA (blue). The dual immunofluorescence procedure used rabbit anti-actin IgG and mouse anti-alpha tubulin IgG as primary antibodies. The secondary antibodies used were Texas Red-conjugated goat, anti-rabbit IgG and FITC-conjugated goat, anti-mouse IgG. The sample was also stained with the DNA-specific dye Hoechst 33342. Scale bar is equal to 20 microns.

Sethi, J.M., Otterbein, L.E., Choi, A.M.K. (2002). Differential modulation by exogenous carbon monoxide of TNF-a stimulated mitogen-activated protein kinase in rat pulmonary artery endothelial cells. Antioxid. Redox Signal. 4 241-58. 

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. 

Suttorp N, Buerke M, Tannert-Otto S et al. (1992) Stimulation of PAF-synthesis in pulmonary artery endothelial cells by Staphylococcus aureus alpha-toxin. In Thromb Res 67 243-252. 

Lind, D. S., Copeland, E. M., Ill, and Souba, W. W. (1993). Endotoxin stimulates arginine transport in pulmonary artery endothelial cells. Surgery 114, 199-205. 

S-allyl cysteine (SAC) may be useful for prevention of aUierosclerosis and can protect vascular endothelial cells from injury caused by oxidized LDL. Pulmonary artery endothelial cells pre-incubated with S-allylcysteine (0.1, 1, 10 and 20 mM) at 37°C and 5% CO2 for 24 h, washed, and then exposed to 0.1 m ml oxidized LDL for 24 h, significantly prevented membrane damage, loss of cell viability and lipid peroxidation. This indicates that SAC can protect vascular endothelial cells from injury caused by oxidized LDL, and suggest tiiat it may be useful for prevention of atherosclerosis [72]. 

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... 

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]. 

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. 

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