Crossref journal-article
Oxford University Press (OUP)
The Journal of Immunology (286)
Abstract

Abstract Platelet/endothelial cell adhesion molecule-1 (PECAM-1; CD31), a member of the Ig superfamily, is expressed strongly at endothelial cell-cell junctions, on platelets, and on most leukocytes. CD31 has been postulated to play a role in vasculogenesis and angiogenesis, and has been implicated as a key mediator of the transendothelial migration of leukocytes. To further define the physiologic role of CD31, we used targeted gene disruption of the CD31 gene in embryonic stem cells to generate CD31-deficient mice. CD31-deficient mice (CD31KO) are viable and born at the expected Mendelian frequency, remain healthy, and exhibit no obvious vascular developmental defects. In response to inflammatory challenge, polymorphonuclear leukocytes of CD31KO mice are arrested between the vascular endothelium and the basement membrane of inflammatory site mesenteric microvessels, confirming a role for CD31 in the migration of neutrophils through the subendothelial extracellular matrix. Normal numbers of leukocytes are recovered from inflammatory sites in CD31KO mice, however, suggesting that the defect in leukocyte migration across basal lamina observed in the absence of CD31 may be compensated for by the use of other adhesion molecules, or possibly an increased rate of migration. Homing of T lymphocytes in vivo is normal, and CD31KO mice are able to mount a cutaneous hypersensitivity response normally. In addition, CD31-mediated homophilic adhesion does not appear to play a role in platelet aggregation in vitro. This study provides genetic evidence that CD31 is involved in transbasement membrane migration, but does not play an obligatory role in either vascular development or leukocyte migration.

Bibliography

Duncan, G. S., Andrew, D. P., Takimoto, H., Kaufman, S. A., Yoshida, H., Spellberg, J., Luis de la Pompa, J., Elia, A., Wakeham, A., Karan-Tamir, B., Muller, W. A., Senaldi, G., Zukowski, M. M., & Mak, T. W. (1999). Genetic Evidence for Functional Redundancy of Platelet/Endothelial Cell Adhesion Molecule-1 (PECAM-1): CD31-Deficient Mice Reveal PECAM-1-Dependent and PECAM-1-Independent Functions. The Journal of Immunology, 162(5), 3022–3030.

Authors 14
  1. Gordon S Duncan (first)
  2. David P Andrew (additional)
  3. Hiroaki Takimoto (additional)
  4. Stephen A Kaufman (additional)
  5. Hiroki Yoshida (additional)
  6. Jason Spellberg (additional)
  7. José Luis de la Pompa (additional)
  8. Andrew Elia (additional)
  9. Andrew Wakeham (additional)
  10. Barbara Karan-Tamir (additional)
  11. William A Muller (additional)
  12. Giorgio Senaldi (additional)
  13. Mark M Zukowski (additional)
  14. Tak W Mak (additional)
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Dates
Type When
Created 2 years, 8 months ago (Dec. 31, 2022, 10:12 a.m.)
Deposited 5 months, 1 week ago (March 30, 2025, 1:50 p.m.)
Indexed 3 days, 23 hours ago (Sept. 3, 2025, 7:09 a.m.)
Issued 26 years, 6 months ago (March 1, 1999)
Published 26 years, 6 months ago (March 1, 1999)
Published Online 26 years, 6 months ago (March 1, 1999)
Published Print 26 years, 6 months ago (March 1, 1999)
Funders 0

None

@article{Duncan_1999, title={Genetic Evidence for Functional Redundancy of Platelet/Endothelial Cell Adhesion Molecule-1 (PECAM-1): CD31-Deficient Mice Reveal PECAM-1-Dependent and PECAM-1-Independent Functions}, volume={162}, ISSN={1550-6606}, url={http://dx.doi.org/10.4049/jimmunol.162.5.3022}, DOI={10.4049/jimmunol.162.5.3022}, number={5}, journal={The Journal of Immunology}, publisher={Oxford University Press (OUP)}, author={Duncan, Gordon S and Andrew, David P and Takimoto, Hiroaki and Kaufman, Stephen A and Yoshida, Hiroki and Spellberg, Jason and Luis de la Pompa, José and Elia, Andrew and Wakeham, Andrew and Karan-Tamir, Barbara and Muller, William A and Senaldi, Giorgio and Zukowski, Mark M and Mak, Tak W}, year={1999}, month=mar, pages={3022–3030} }