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Role of alpha4 integrin and VCAM-1 in CD18-independent neutrophil migration across mouse cardiac endothelium.
Circ Res. 2002 Mar 22; 90(5):562-9.CircR

Abstract

Myocardial damage due to reperfusion of ischemic tissue is caused primarily by infiltrating neutrophils. Although leukocyte beta2 integrins (CD18) play a critical role, significant neutrophil emigration persists when CD18 is neutralized or absent. This study examined the role of leukocyte beta1 integrin (alpha4) and its endothelial ligand VCAM-1 in CD18-independent neutrophil migration across cardiac endothelium. In a mouse model of myocardial ischemia and reperfusion, we show that compared with wild-type mice, neutrophil infiltration efficiency was reduced by 50% in CD18-null mice; in both types of mice, myocardial VCAM-1 staining increased after reperfusion. In wild-type mice, antibodies against CD18, ICAM-1 (an endothelial ligand for CD18), or VCAM-1 given 30 minutes before ischemia did not block neutrophil emigration at 3 hours reperfusion. Although anti-VCAM-1 attenuated neutrophil emigration by 90% in CD18-null mice, it did not diminish myocardial injury. To determine if CD18-independent neutrophil emigration was a tissue-specific response, we used isolated peripheral blood neutrophils from wild-type or CD18-null mice and showed neutrophil migration across lipopolysaccharide-activated cultured cardiac endothelium is CD18-independent, whereas migration across endothelium obtained from inferior vena cava is CD18-dependent. Consistent with our in vivo findings, migration of CD18-deficient neutrophils on cardiac endothelial monolayers is blocked by antibodies against alpha4 integrin or VCAM-1. We conclude tissue-specific differences in endothelial cells account, at least partially, for CD18-independent neutrophil infiltration in the heart.

Authors+Show Affiliations

Department of Immunology, Walter Reed Army Institute of Research, Silver Spring, Md, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

11909820

Citation

Bowden, Robert A., et al. "Role of Alpha4 Integrin and VCAM-1 in CD18-independent Neutrophil Migration Across Mouse Cardiac Endothelium." Circulation Research, vol. 90, no. 5, 2002, pp. 562-9.
Bowden RA, Ding ZM, Donnachie EM, et al. Role of alpha4 integrin and VCAM-1 in CD18-independent neutrophil migration across mouse cardiac endothelium. Circ Res. 2002;90(5):562-9.
Bowden, R. A., Ding, Z. M., Donnachie, E. M., Petersen, T. K., Michael, L. H., Ballantyne, C. M., & Burns, A. R. (2002). Role of alpha4 integrin and VCAM-1 in CD18-independent neutrophil migration across mouse cardiac endothelium. Circulation Research, 90(5), 562-9.
Bowden RA, et al. Role of Alpha4 Integrin and VCAM-1 in CD18-independent Neutrophil Migration Across Mouse Cardiac Endothelium. Circ Res. 2002 Mar 22;90(5):562-9. PubMed PMID: 11909820.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of alpha4 integrin and VCAM-1 in CD18-independent neutrophil migration across mouse cardiac endothelium. AU - Bowden,Robert A, AU - Ding,Zhi-Ming, AU - Donnachie,Elizabeth M, AU - Petersen,Thomas K, AU - Michael,Lloyd H, AU - Ballantyne,Christie M, AU - Burns,Alan R, PY - 2002/3/23/pubmed PY - 2002/3/27/medline PY - 2002/3/23/entrez SP - 562 EP - 9 JF - Circulation research JO - Circ Res VL - 90 IS - 5 N2 - Myocardial damage due to reperfusion of ischemic tissue is caused primarily by infiltrating neutrophils. Although leukocyte beta2 integrins (CD18) play a critical role, significant neutrophil emigration persists when CD18 is neutralized or absent. This study examined the role of leukocyte beta1 integrin (alpha4) and its endothelial ligand VCAM-1 in CD18-independent neutrophil migration across cardiac endothelium. In a mouse model of myocardial ischemia and reperfusion, we show that compared with wild-type mice, neutrophil infiltration efficiency was reduced by 50% in CD18-null mice; in both types of mice, myocardial VCAM-1 staining increased after reperfusion. In wild-type mice, antibodies against CD18, ICAM-1 (an endothelial ligand for CD18), or VCAM-1 given 30 minutes before ischemia did not block neutrophil emigration at 3 hours reperfusion. Although anti-VCAM-1 attenuated neutrophil emigration by 90% in CD18-null mice, it did not diminish myocardial injury. To determine if CD18-independent neutrophil emigration was a tissue-specific response, we used isolated peripheral blood neutrophils from wild-type or CD18-null mice and showed neutrophil migration across lipopolysaccharide-activated cultured cardiac endothelium is CD18-independent, whereas migration across endothelium obtained from inferior vena cava is CD18-dependent. Consistent with our in vivo findings, migration of CD18-deficient neutrophils on cardiac endothelial monolayers is blocked by antibodies against alpha4 integrin or VCAM-1. We conclude tissue-specific differences in endothelial cells account, at least partially, for CD18-independent neutrophil infiltration in the heart. SN - 1524-4571 UR - https://www.unboundmedicine.com/medline/citation/11909820/Role_of_alpha4_integrin_and_VCAM_1_in_CD18_independent_neutrophil_migration_across_mouse_cardiac_endothelium_ L2 - https://www.ahajournals.org/doi/10.1161/01.res.0000013835.53611.97?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -