Human leukocytes express ephrinB2 which activates microvascular endothelial cells

David O. Zamora; Bobby Babra; Yuzhen Pan; Stephen R. Planck; James T. Rosenbaum

doi:10.1016/j.cellimm.2006.10.001

Human leukocytes express ephrinB2 which activates microvascular endothelial cells

David O. Zamora
, Bobby Babra
, Yuzhen Pan
, Stephen R. Planck
, James T. Rosenbaum

Ophthalmology

Research output: Contribution to journal › Article › peer-review

21 Scopus citations

Abstract

EphrinB2-EphB4 interaction modulates the migration/adhesion of various cell types, including endothelial cells (EC) and peripheral blood leukocytes (PBLs). We hypothesize that the Ephrin/Eph signaling mechanism plays a role in mediating EC/leukocyte interactions during inflammation. PBLs were isolated from human blood, stimulated with inflammatory mediators, and total RNA or protein assayed for EphrinB2 expression. PBLs demonstrated differential expression profiles of EphrinB2 mRNA or protein, depending on cell subtype and stimulus. Human iris tissue and iris EC (HIEC) were examined for the expression of EphB4 mRNA and protein. Some blood vessels were EphB4⁺, while stimulation of purified HIEC did not alter their expression of EphB4. HIEC treated with sEphrinB2/Fc from 0 to 60 min did exhibit changes in their phospho-Erk1/2 levels. These observations indicate that stimulated lymphocytes express EphrinB2, which has the potential to activate EC. This suggests a novel mechanism by which EC and lymphocytes communicate to regulate cell activation/migration during inflammation.

Original language	English (US)
Pages (from-to)	99-109
Number of pages	11
Journal	Cellular Immunology
Volume	242
Issue number	2
DOIs	https://doi.org/10.1016/j.cellimm.2006.10.001
State	Published - Aug 2006

Funding

This project was supported by NEI Grants EY011548, EY06477, EY06484, EY10572; by Research to Prevent Blindness awards to JTR, SRP, and the Casey Eye Institute; by Tartar Trust Research Fellowship grants (Oregon Science Foundation, Portland, OR) to DOZ. This work was presented, in part, in a paper session at the Association for Research in Vision and Ophthalmology annual conference, May 4, 2003, Ft. Lauderdale, FL.

Funders	Funder number
National Eye Institute and Casey Eye Institute
Oregon Health & Science University Foundation
Tartar Trust
National Eye Institute and Casey Eye Institute	EY011548, EY06477, EY10572, EY06484
Research to Prevent Blindness

Keywords

Artery
Diapedesis
Endothelial cells
Eph
Ephrin
Extravasation
Inflammation
Iris
Leukocyte
Vein

ASJC Scopus subject areas

Immunology

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10.1016/j.cellimm.2006.10.001

Cite this

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title = "Human leukocytes express ephrinB2 which activates microvascular endothelial cells",

abstract = "EphrinB2-EphB4 interaction modulates the migration/adhesion of various cell types, including endothelial cells (EC) and peripheral blood leukocytes (PBLs). We hypothesize that the Ephrin/Eph signaling mechanism plays a role in mediating EC/leukocyte interactions during inflammation. PBLs were isolated from human blood, stimulated with inflammatory mediators, and total RNA or protein assayed for EphrinB2 expression. PBLs demonstrated differential expression profiles of EphrinB2 mRNA or protein, depending on cell subtype and stimulus. Human iris tissue and iris EC (HIEC) were examined for the expression of EphB4 mRNA and protein. Some blood vessels were EphB4+, while stimulation of purified HIEC did not alter their expression of EphB4. HIEC treated with sEphrinB2/Fc from 0 to 60 min did exhibit changes in their phospho-Erk1/2 levels. These observations indicate that stimulated lymphocytes express EphrinB2, which has the potential to activate EC. This suggests a novel mechanism by which EC and lymphocytes communicate to regulate cell activation/migration during inflammation.",

keywords = "Artery, Diapedesis, Endothelial cells, Eph, Ephrin, Extravasation, Inflammation, Iris, Leukocyte, Vein",

author = "Zamora, \{David O.\} and Bobby Babra and Yuzhen Pan and Planck, \{Stephen R.\} and Rosenbaum, \{James T.\}",

note = "Funding Information: This project was supported by NEI Grants EY011548, EY06477, EY06484, EY10572; by Research to Prevent Blindness awards to JTR, SRP, and the Casey Eye Institute; by Tartar Trust Research Fellowship grants (Oregon Science Foundation, Portland, OR) to DOZ. This work was presented, in part, in a paper session at the Association for Research in Vision and Ophthalmology annual conference, May 4, 2003, Ft. Lauderdale, FL. ",

year = "2006",

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doi = "10.1016/j.cellimm.2006.10.001",

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journal = "Cellular Immunology",

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AU - Zamora, David O.

AU - Babra, Bobby

AU - Pan, Yuzhen

AU - Planck, Stephen R.

AU - Rosenbaum, James T.

N1 - Funding Information: This project was supported by NEI Grants EY011548, EY06477, EY06484, EY10572; by Research to Prevent Blindness awards to JTR, SRP, and the Casey Eye Institute; by Tartar Trust Research Fellowship grants (Oregon Science Foundation, Portland, OR) to DOZ. This work was presented, in part, in a paper session at the Association for Research in Vision and Ophthalmology annual conference, May 4, 2003, Ft. Lauderdale, FL.

PY - 2006/8

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N2 - EphrinB2-EphB4 interaction modulates the migration/adhesion of various cell types, including endothelial cells (EC) and peripheral blood leukocytes (PBLs). We hypothesize that the Ephrin/Eph signaling mechanism plays a role in mediating EC/leukocyte interactions during inflammation. PBLs were isolated from human blood, stimulated with inflammatory mediators, and total RNA or protein assayed for EphrinB2 expression. PBLs demonstrated differential expression profiles of EphrinB2 mRNA or protein, depending on cell subtype and stimulus. Human iris tissue and iris EC (HIEC) were examined for the expression of EphB4 mRNA and protein. Some blood vessels were EphB4+, while stimulation of purified HIEC did not alter their expression of EphB4. HIEC treated with sEphrinB2/Fc from 0 to 60 min did exhibit changes in their phospho-Erk1/2 levels. These observations indicate that stimulated lymphocytes express EphrinB2, which has the potential to activate EC. This suggests a novel mechanism by which EC and lymphocytes communicate to regulate cell activation/migration during inflammation.

AB - EphrinB2-EphB4 interaction modulates the migration/adhesion of various cell types, including endothelial cells (EC) and peripheral blood leukocytes (PBLs). We hypothesize that the Ephrin/Eph signaling mechanism plays a role in mediating EC/leukocyte interactions during inflammation. PBLs were isolated from human blood, stimulated with inflammatory mediators, and total RNA or protein assayed for EphrinB2 expression. PBLs demonstrated differential expression profiles of EphrinB2 mRNA or protein, depending on cell subtype and stimulus. Human iris tissue and iris EC (HIEC) were examined for the expression of EphB4 mRNA and protein. Some blood vessels were EphB4+, while stimulation of purified HIEC did not alter their expression of EphB4. HIEC treated with sEphrinB2/Fc from 0 to 60 min did exhibit changes in their phospho-Erk1/2 levels. These observations indicate that stimulated lymphocytes express EphrinB2, which has the potential to activate EC. This suggests a novel mechanism by which EC and lymphocytes communicate to regulate cell activation/migration during inflammation.

KW - Artery

KW - Diapedesis

KW - Endothelial cells

KW - Eph

KW - Ephrin

KW - Extravasation

KW - Inflammation

KW - Iris

KW - Leukocyte

KW - Vein

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ER -

Human leukocytes express ephrinB2 which activates microvascular endothelial cells

Abstract

Funding

Keywords

ASJC Scopus subject areas

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