Heterogeneity of Expression of E- and P-Selectins In Vivo

Eppihimer, Michael J.; Wolitzky, Barry A.; Anderson, Donald C.; Labow, Mark; Granger, D. Neil

doi:10.1161/01.res.79.3.560

Cited by 295 publications

(293 citation statements)

References 32 publications

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“…Expression of the adhesion molecules P-selectin and VCAM-1 were quantified using a modified dualradiolabeled Ab technique (21,24). The Abs RB40.34 (against P-selectin) and 429 (MVCAM.A) (against VCAM-1) were labeled with 125 I.…”

Section: Quantitation Of Endothelial Activationmentioning

confidence: 99%

“…The Abs A110-1 (a rat IgG1, isotype standard) and R35-95 (a rat IgG2a, isotype control Ig) were labeled with 131 I. In both cases, the Abs were labeled using the IodoGen method, as previously described (21,24). A110-1 and R35-95 were used to detect nonspecific binding in the murine system.…”

Section: Quantitation Of Endothelial Activationmentioning

confidence: 99%

“…It has been previously demonstrated that this approach provides reliable quantitative values of adhesion molecule expression and that radiolabeled binding Ab can be displaced specifically with sufficient amounts of unlabeled Ab. The technique is sufficiently sensitive that very small, basal levels of P-selectin can be detected in wild-type mice relative to P-selectin-deficient mice where values are zero (24,25).…”

Section: Quantitation Of Endothelial Activationmentioning

confidence: 99%

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Lipopolysaccharide-Induced Leukocyte-Endothelial Cell Interactions: A Role for CD14 Versus Toll-Like Receptor 4 Within Microvessels

Andonegui

Goyert

Kubes

2002

The Journal of Immunology

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The objective of this study was to systematically assess leukocyte-endothelial cell interactions in vivo in response to LPS in CD14-deficient (CD14−/−) and Toll-like receptor 4-deficient (TLR4d; C3H/HeJ) mice. Local injection of LPS (0.05 μg/kg) into muscle at a concentration that did not cause systemic effects produced a significant reduction in the speed with which leukocytes roll and a substantial increase in leukocyte adhesion and emigration 4 h postinjection. There was no response to LPS in the muscle microvasculature of CD14−/− mice or TLR4d animals. Systemic LPS induced leukopenia and significant sequestration of neutrophils in lungs in wild-type mice but not in CD14−/− or TLR4d mice. P-selectin expression was examined in numerous mouse organs using a dual radiolabeling mAb technique. The results revealed a 20- to 50-fold increase in P-selectin expression in response to LPS in all wild-type tissues examined but no response in any TLR4d tissues. Surprisingly, there was consistently a partial, significant increase in P-selectin expression in numerous microvasculatures including skin and pancreas, but no increase in P-selectin was detected in lung, muscle, and other organs in CD14−/− mice in response to LPS. Next, the skin and muscle microcirculation were visualized using intravital microscopy after systemic LPS treatment, and the results confirmed a CD14-independent mechanism of leukocyte sequestration in skin but not muscle. In summary, our results suggest that the LPS-induced leukocyte sequestration to some tissues is entirely dependent on both CD14 and TLR4 but there are CD14-independent, TLR4-dependent endothelial cell responses in some microvascular beds.

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Section: Quantitation Of Endothelial Activationmentioning

confidence: 99%

Section: Quantitation Of Endothelial Activationmentioning

confidence: 99%

Section: Quantitation Of Endothelial Activationmentioning

confidence: 99%

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Lipopolysaccharide-Induced Leukocyte-Endothelial Cell Interactions: A Role for CD14 Versus Toll-Like Receptor 4 Within Microvessels

Andonegui

Goyert

Kubes

2002

The Journal of Immunology

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“…We have previously demonstrated that in vivo P-selectin expression increases in mesenteric venules of the rat 6 hr after abdominal irradiation with 10 Gy [12]. The heterogeneity in constitutive and induced P-selectin expression in the different vascular beds [13] suggests that its role in acute inflammation may depend on the tissue in which damage occurs.…”

Section: Introductionmentioning

confidence: 99%

Role of P‐selectin in radiation‐induced intestinal inflammatory damage

Mollà

Gironella

Salas

et al. 2001

Intl Journal of Cancer

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SUMMARY The aims of our study were to characterize the dose-and time-dependent changes in endothelial P-selectin expression and the role of this adhesion molecule as a mediator of radiation-induced inflammation. For that purpose, endothelial P-selectin expression was measured by the radiolabeled antibody technique in control and irradiated mice at 2, 6, and 24 hr following abdominal irradiation with 4 or 10 Gy; leukocyte endothelial cell interactions were assessed using intravital microscopy in intestinal venules following irradiation at the aforementioned doses and times in C57BL/6 and P-selectindeficient mice. In wild-type mice, radiation induced a time-and dose-dependent upregulation of P-selectin and a significant increase in the flux of rolling leukocytes 2 hr after irradiation. Irradiation induced a significant increase in leukocyte adhesion that was dosedependent. Following irradiation, P-selectin-deficient mice did not show any increase in leukocyte rolling but did demonstrate a response in leukocyte adhesion similar to that of the wild-type mice. Radiation-induced dose-dependent histological inflammatory damage that did not differ between P-selectin-deficient and wild-type mice. We conclude that P-selectin is up-regulated following irradiation and is a key molecular determinant of leukocyte rolling but not leukocyte adhesion in this inflammatory condition. Therefore, isolated neutralization of this adhesion molecule is not an effective means for preventing radiation-induced inflammation.

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“…There are several other surface markers that also show promise as EC targets such as intercellular adhesion molecule 1 (ICAM-1), lectin-like oxidized LDL receptor (LOX-1), and P-selectin (18). P-selectin is constitutively expressed on vascular endothelium with lung ECs having the highest level of expression.…”

Section: Surface Properties and Uptake Mechanisms Of Macromolecules Omentioning

confidence: 99%

Targeted Delivery of Nucleic Acid-Based Therapeutics to the Pulmonary Circulation

Kuruba

Wilson

Gao

et al. 2009

AAPS J

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Abstract. Targeted delivery of functional nucleic acids (genes and oligonucleotides) to pulmonary endothelium may become a novel therapy for the treatment of various types of lung diseases. It may also provide a new research tool to study the functions and regulation of novel genes in pulmonary endothelium. Its success is largely dependent on the development of a vehicle that is capable of efficient pulmonary delivery with minimal toxicity. This review summarizes the recent progress that has been made in our laboratory along these research directions. Factors that affect pulmonary nucleic acids delivery are also discussed.

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Heterogeneity of Expression of E- and P-Selectins In Vivo

Cited by 295 publications

References 32 publications

Lipopolysaccharide-Induced Leukocyte-Endothelial Cell Interactions: A Role for CD14 Versus Toll-Like Receptor 4 Within Microvessels

Lipopolysaccharide-Induced Leukocyte-Endothelial Cell Interactions: A Role for CD14 Versus Toll-Like Receptor 4 Within Microvessels

Role of P‐selectin in radiation‐induced intestinal inflammatory damage

Targeted Delivery of Nucleic Acid-Based Therapeutics to the Pulmonary Circulation

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