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ELAM-1 expression

Selectins mediate the initial weak tethering of neutrophils to the endothelial wall. This results in characteristic rolling of the neutrophils along the endothelium under conditions of heightened shear force. L-selectin (LECAM-1) is constitutively expressed on neutrophils (Lasky, 1991), whereas E-selectin (ELAM-1) expression is induced on endothelial cells by exposure to endotoxin, TNFa or... [Pg.26]

Montefort, S., Roche, W.R, Howarth, P.H., Djukanovic, R, Gratziou, C., Carroll, M., Smith, L., Britten, K.M., Haskard, D., Lee, T.H. and Holgate, S.T. (1992). Intercellular adhesion molecule-1 (ICAM-1) and endothelial leukocyte adhesion molecule-1 (ELAM-1) expression in the bronchial mucosa of normal and asthmatic subjects. Eur. Respir. J. 5, 815-823. [Pg.96]

Results are expressed as means S.E. of 4-8 experiments. HUVECs were preincubated with the various concentrations of baicalein for 1 h at 37° C, and then thrombin (10 U/mL) was added and the mixture was further incubated for 6 h (ELAM-1 expression) or 24 h (ICAM-1 expression) at 37 C. [Pg.71]

Fig. ( 3). Effects of baicalein on TRAP-induced ELAM-1 expression in cultured HUVECs. Fig. ( 3). Effects of baicalein on TRAP-induced ELAM-1 expression in cultured HUVECs.
These findings suggest that the inhibitory effects of baicalein on thrombin-induced ELAM-1 and ICAM-1 expression, or TRAP-induced ELAM-1 expression, may be due to the inhibition of PKC activation. I previously reported that baicalein had potent anti-allergic and... [Pg.71]

Initial tumor growth, during which the anti-inflammatory activity of lL-10 inhibits reactive cells and their proinflammatory cytokine production, is followed by ELAM-1 expression [55], possibly induced directly by lL-10 in peripheral tumor microvessels [56]. The resulting neutrophil influx and interaction with ECs play a key role in leading to a delayed, but efficacious antitumor reaction with complete tumor eradication. [Pg.187]

Corkill, M.M., Kirkham, B.W., Haskard, D.O., Barbatis, C., Gibson, T. and Panayi, G.S. (1991). Gold treatment of rheumatoid arthritis decreases synovial expression of the endothelial leucocyte receptor ELAM-1. J. Rheumatol. 18, 1453-1460. [Pg.109]

In the area of copper metabolism, four topics are covered bacterial copper transport reviewed by Huat Lu and Sohoz copper P-type ATPases reviewed by Voskoboinik, Camakaris, and Mercer copper chaperones reviewed by Stine Elam et al. and copper metaUoregulation of gene expression reviewed by Winge. An important related topic is the link between copper and iron metabolism. In this area, Kosman has reviewed the multicopper oxidase enzymes, such as FetSp and ceruloplasmin, which catalyze the conversion of iron(II) to iron(III) in preparation for its specific transport by partner transporter proteins. [Pg.504]

Upregulation of adhesion molecules has been documented in human stroke patients [7]. It was demonstrated that leukocytes from patients suffering an ischemic stroke or transient ischemic attack showed increased CDl la expression within 72 hours of the onset of symptoms [123]. Increased ICAM-1 expression on the surface of vessels fi om cerebral cortical infarcts was detected in four patients [124]. In some studies, soluble isoforms of adhesion molecules shed fi om the surfaces of activated cells were quantified in serum. Serum endothelial-leukocyte adhesion molecule-1 (ELAM-1, E-selectin) levels increased up to 24 hours after stroke. Similar increases were observed in serum vascular cell adhesion molecule-1 (VCAM-1) levels and these increases were sustained up to 5 days [125]. In contrast, serum ICAM-1 levels in acute ischemic stroke patients have been found to be lower than or the same as those of asymptomatic control subjects matched for age, sex, and vascular risk factors [125,126]. The reason not to detect an increase in serum levels of adhesion molecules might be due to the late enrolling of patients. Once adhesion molecules bind to leukocytes and endothelial cells, they can no longer be detected in serum [7]. [Pg.193]

ELAM-1 and lCAM-1 expressions in cultured human umbilical endothelial cells... [Pg.434]

Thiid passage culture s of HUVECs were used in a 5% COj atmosphere at 37°C. Expressions of ELAM-1 and ICAM-1 in cultured HUVECs were determined by cell enzyme-linked immunoassay TNF- a 5 ngAnl, IL-1 / 20 ng/ml. [Pg.434]

The innervation of the lymphoid vasculature by substance P-containing neurons and the ability of substance P to enhance lymph tissue blood flow (Lundbeig et al., 1985) suggest that substance P may alter lymphocyte traffic . Substance P induces the expression of endothelial leukocyte adhesion molecule 1 (ELAM-1) on microvascular endothelial cells (Matis et al., 1990) and may similarly affect the expression of adhesion molecules on lymphocytes. Infusion of substance P has been shown to increase lymph flow and lymphocyte traffic in sheep lymph nodes (Moore etal., 1989). [Pg.131]

Increased cytokine production may also play a role in silica-induced autoimmune vascular disease. Adhesion molecule expression is elevated on vascular endothelial cells in response to TNF-a and IL-1. Adhesion molecules such as endothelial leukocyte adhesion molecule-1 (ELAM-1) and intercellular adhesion molecule-1 (ICAM-1) recruit inflammatory cells to specific sites on the vascular endothelium, and it has been hypothesized that vascular pathology following silica exposure may be the result of this interaction (Nowack et al., 1998). IFN-y is expressed at elevated levels by lymphocytes in silicotic thoracic lymph nodes and may be responsible for the long-lasting inducible nitric oxide synthase (iNOS) expression in these tissues (Friedetzky et al., 2002). The increase in IFN-y may also cause a shift towards a dominant Thl response, contributing to the maintenance of a chronic inflammatory state in silica-containing lymph nodes (Gam et al., 2000). [Pg.128]

Table 14. Effects of PKC inhibitor H7 and baicalein on ELAM-1 and ICAM-1 expression induced by PMA, thrombin and TRAP in cultured HUVECs1... Table 14. Effects of PKC inhibitor H7 and baicalein on ELAM-1 and ICAM-1 expression induced by PMA, thrombin and TRAP in cultured HUVECs1...

See other pages where ELAM-1 expression is mentioned: [Pg.70]    [Pg.71]    [Pg.290]    [Pg.192]    [Pg.82]    [Pg.106]    [Pg.70]    [Pg.318]    [Pg.58]    [Pg.58]    [Pg.540]    [Pg.872]    [Pg.369]    [Pg.125]    [Pg.44]    [Pg.192]    [Pg.61]    [Pg.213]    [Pg.715]    [Pg.214]    [Pg.218]    [Pg.7]    [Pg.70]    [Pg.71]    [Pg.289]    [Pg.290]    [Pg.291]    [Pg.187]    [Pg.192]    [Pg.392]   
See also in sourсe #XX -- [ Pg.30 , Pg.70 , Pg.71 , Pg.291 ]

See also in sourсe #XX -- [ Pg.70 , Pg.71 , Pg.291 ]




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ELAM-1 expression baicalein effect

ELAM-1 expression induction by TRAP

Elame

TRAP-induced ELAM-1 expression

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