Molecular cloning and analysis of in vivo expression of murine P- selectin

We, Sanders; Wilson, Raymond W.; Ballantyne, C.M.; Beaudet, A. L.

doi:10.1182/blood.v80.3.795.795

Cited by 157 publications

(26 citation statements)

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“…Certainly, another mechanism by which LPS promotes acute lung inflammation is by upregulating the expression of CAMs. Thus, the transcript levels of P-selectin, E-selectin, ICAM-1 and VCAM-1 are augmented in the lung, with peaks observed at 3-6 h after exposure to LPS (Sanders et al, 1992;Fries et al, 1993;Beck-Schimmer et al, 1997;Panes et al, 1999). In keeping with these studies, we found that i.t.…”

Section: Discussionsupporting

confidence: 86%

“…The lung tissue samples were obtained at 4 h postchallenge. This time point for measurements of CAM's mRNA was selected from previous reports (Sanders et al, 1992;Fries et al, 1993;Beck-Schimmer et al, 1997). Total RNA was extracted from lung tissue homogenates by using TriPure Isolation Reagent (Roche Applied Science, Indianapolis, IN, U.S.A.).…”

Section: Lps-induced Lung Inflammationmentioning

confidence: 99%

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Erythromycin exerts in vivo anti‐inflammatory activity downregulating cell adhesion molecule expression

Sanz

Nabah

Cerdá-Nicolás

et al. 2005

British J Pharmacology

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1 Macrolides have long been used as anti-bacterial agents; however, there is some evidence that may exert anti-inflammatory activity. Therefore, erythromycin was used to characterize the mechanisms involved in their in vivo anti-inflammatory activity. 2 Erythromycin pretreatment (30 mg kg À1 day À1 for 1 week) reduced the lipopolysaccharide (LPS; intratracheal, 0.4 mg kg À1 )-induced increase in neutrophil count and elastase activity in the bronchoalveolar lavage fluid (BALF) and lung tissue myeloperoxidase activity, but failed to decrease tumor necrosis factor-a and macrophage-inflammatory protein-2 augmented levels in BALF. Erythromycin pretreatment also prevented lung P-selectin, E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) mRNA upregulation in response to airway challenge with LPS. 3 Mesentery superfusion with LPS (1 mg ml À1 ) induced a significant increase in leukocyte-endothelial cell interactions at 60 min. Erythromycin pretreatment abolished the increases in these parameters. 4 LPS exposure of the mesentery for 4 h caused a significant increase in leukocyte rolling flux, adhesion and emigration, which were inhibited by erythromycin by 100, 93 and 95%, respectively. 5 Immunohistochemical analysis showed that LPS exposure of the mesentery for 4 h caused a significant enhancement in P-selectin, E-selectin, ICAM-1 and VCAM-1 expression that was downregulated by erythromycin pretreatment. 6 Flow cytometry analysis indicated that erythromycin pretreatment inhibited LPS-induced CD11b augmented expression in rat neutrophils. 7 In conclusion, erythromycin inhibits leukocyte recruitment in the lung and this effect appears mediated through downregulation of CAM expression. Therefore, macrolides may be useful in the control of neutrophilic pulmonary diseases.

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Section: Discussionsupporting

confidence: 86%

Section: Lps-induced Lung Inflammationmentioning

confidence: 99%

Erythromycin exerts in vivo anti‐inflammatory activity downregulating cell adhesion molecule expression

Sanz

Nabah

Cerdá-Nicolás

et al. 2005

British J Pharmacology

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“…Endothelial selectins are not constitutively expressed, with the exception of E-selectin in the cutaneous microcirculation (Norton et al, 1991). Thus, the capacity of LPS to upregulate P-and E-selectin expression in vivo (Gotsch et al, 1994;Labow et al, 1994;Mayadas et al, 1993;Sanders et al, 1992) could explain the inhibitory eect of monoclonal antibodies (mAbs) against these molecules on LPS-induced neutrophil recruitment. It is not known, however, whether selectins are similarly required for neutrophil accumulation induced by a directacting in¯ammatory mediator such as a CXC chemokine.…”

Section: Introductionmentioning

confidence: 99%

Dominant role of L‐ and P‐selectin in mediating CXC chemokine‐induced neutrophil migration in vivo

Miotla

Ridger

Hellewell

2001

British J Pharmacology

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1 The role of selectins in neutrophil emigration in response to the CXC chemokines KC and MIP-2 was investigated in wild type and P-selectin de®cient mice. 2 Intrapleural injection of KC or MIP-2 induced a rapid and speci®c neutrophil accumulation. Emigration 2 h after KC or MIP-2 was reduced 83 ± 88% by anti-L-selectin mAb and 53 ± 63% by anti-P-selectin mAb. Co-administration of anti-L-and P-selectin mAbs abolished neutrophil migration induced by either chemokine. 3 An anti-E-selectin mAb tested alone did not aect KC-induced neutrophil migration after 2 or 4 h. Moreover, anti-E-selectin did not have an additive inhibitory eect on KC-induced neutrophil migration compared with P-selectin blockade alone. This was found when neutrophil migration was measured at 2 and 4 h after KC. 4 Despite a blood neutrophilia, neutrophil migration at 2 and 4 h after KC was markedly smaller (by approximately 90%) in P-selectin de®cient mice compared with wild type animals. Responses at both time points were not decreased further in animals given E-selectin mAb but were reduced to the PBS control level in the presence of anti-L-selectin. 5 In vitro study of cultured murine endothelial cells demonstrated that KC can directly increase cell surface P-selectin expression. 6 These data suggest that CXC chemokine-induced neutrophil accumulation is dependent on both neutrophil L-selectin and a rapid upregulation of endothelial P-selectin but there is no evidence for E-selectin induction.

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“…From there it can rapidly be brought to the cell surface after exposure to thrombin, histamine, complement 5a, Ca 2ϩ ionophores, or adenosine diphosphate (21)(22)(23)(24). In mice, endotoxin injection has also been shown to induce P-selectin expression in liver, heart, lung, and kidney (25). Surface P-selectin expression is downregulated by internalization, degradation, and to a smaller extent by shedding into the plasma (22,24).…”

mentioning

confidence: 99%

Platelet, but not endothelial, P‐selectin is critical for neutrophil‐mediated acute postischemic renal failure

Forlow²,

2001

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In a neutrophil-dependent model of acute postischemic renal failure (APRF), eliminating or blocking P-selectin reduces postischemic neutrophil infiltration and preserves kidney function. This study was designed to identify the role of platelet vs. endothelial P-selectin in APRF. Using wild-type (wt) and P-selectin-deficient (P-/-) mice, we generated chimeric mice by bone marrow transplantation. Chimeric mice exclusively expressed either platelet (Plt-P) or endothelial P-selectin (EC-P). APRF was induced by bilateral renal ischemia in situ (32 min), followed by reperfusion; 48 h after reperfusion, EC-P had significantly lower creatinine concentrations (twofold over sham) than Plt-P (eightfold over sham). Compared with wt, protection from renal failure in EC-P was similar to that observed in P-/-. Plt-P and EC-P demonstrated similar overall postischemic neutrophil infiltration as measured by renal myeloperoxidase activity. However, Plt-P showed massive neutrophil infiltration into outer and inner medulla, similar to that in wt. EC-P had only patchy, more diffuse neutrophil influx. Our study identifies platelet P-selectin as crucial for postischemic neutrophil recruitment into outer and inner medulla, which is detrimental to the development of APRF. This suggests that novel therapeutic strategies for postischemic organ failure could be aimed at neutrophil-platelet interactions.

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Molecular cloning and analysis of in vivo expression of murine P- selectin

Cited by 157 publications

References 0 publications

Erythromycin exerts in vivo anti‐inflammatory activity downregulating cell adhesion molecule expression

Erythromycin exerts in vivo anti‐inflammatory activity downregulating cell adhesion molecule expression

Dominant role of L‐ and P‐selectin in mediating CXC chemokine‐induced neutrophil migration in vivo

Platelet, but not endothelial, P‐selectin is critical for neutrophil‐mediated acute postischemic renal failure

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