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Titolo:
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
Autore:
Duncan, GS; Andrew, DP; Takimoto, H; Kaufman, SA; Yoshida, H; Spellberg, J; de la Pompa, JL; Elia, A; Wakeham, A; Karan-Tamir, B; Muller, WA; Senaldi, G; Zukowski, MM; Mak, TW;
Indirizzi:
Amgen Inst, Toronto, ON M5G 2C1, Canada Amgen Inst Toronto ON Canada M5G 2C1 en Inst, Toronto, ON M5G 2C1, Canada Amgen Boulder, Dept Inflammat, Boulder, CO 80301 USA Amgen Boulder Boulder CO USA 80301 Dept Inflammat, Boulder, CO 80301 USA Univ Toronto, Ontario Canc Inst, Dept Med Biophys, Toronto, ON, Canada Univ Toronto Toronto ON Canada st, Dept Med Biophys, Toronto, ON, Canada Univ Toronto, Ontario Canc Inst, Dept Immunol, Toronto, ON, Canada Univ Toronto Toronto ON Canada c Inst, Dept Immunol, Toronto, ON, Canada Amgen, Thousand Oaks, CA 91320 USA Amgen Thousand Oaks CA USA 91320Amgen, Thousand Oaks, CA 91320 USA Cornell Univ, Coll Med, Dept Pathol, New York, NY 10021 USA Cornell Univ New York NY USA 10021 d, Dept Pathol, New York, NY 10021 USA
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 5, volume: 162, anno: 1999,
pagine: 3022 - 3030
SICI:
0022-1767(19990301)162:5<3022:GEFFRO>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
IN-VIVO; TRANSENDOTHELIAL MIGRATION; LEUKOCYTE EXTRAVASATION; NEUTROPHIL RECRUITMENT; DOWN-REGULATION; KILLER-CELLS; CD31; INTEGRIN; ANGIOGENESIS; ENDOTHELIUM;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
52
Recensione:
Indirizzi per estratti:
Indirizzo: Mak, TW Amgen Inst, 620 Univ Ave, Toronto, ON M5G 2C1, Canada Amgen Inst 620 Univ Ave Toronto ON Canada M5G 2C1 M5G 2C1, Canada
Citazione:
G.S. Duncan et al., "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", J IMMUNOL, 162(5), 1999, pp. 3022-3030

Abstract

Platelet/endothelial cell adhesion molecule-1 (PECAM-1; CD31), a member ofthe 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 heymediator 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 membraneof 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 hemophilic 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 rolein either vascular development or leukocyte migration.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 16:53:50