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Titolo:
LACTOSYLCERAMIDE STIMULATES HUMAN NEUTROPHILS TO UP-REGULATE MAC-1, ADHERE TO ENDOTHELIUM, AND GENERATE REACTIVE OXYGEN METABOLITES IN-VITRO
Autore:
ARAI T; BHUNIA AK; CHATTERJEE S; BULKLEY GB;
Indirizzi:
JOHNS HOPKINS UNIV,SCH MED,DEPT SURG,BLALOCK 685,600 N WOLFE ST BALTIMORE MD 21287 JOHNS HOPKINS UNIV,SCH MED,DEPT SURG BALTIMORE MD 21287 JOHNS HOPKINS UNIV,SCH MED,DEPT PEDIAT BALTIMORE MD 21205 JOHNS HOPKINS UNIV,SCH MED,LIPID RES UNIT BALTIMORE MD 00000
Titolo Testata:
Circulation research
fascicolo: 5, volume: 82, anno: 1998,
pagine: 540 - 547
SICI:
0009-7330(1998)82:5<540:LSHNTU>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
POLYMORPHONUCLEAR LEUKOCYTES; CHEMOTACTIC FACTORS; ACTIVATION; CELLS; ADHESION; GLYCOSPHINGOLIPIDS; EXPRESSION; PHOSPHOLIPASE; LOCALIZATION; OXIDASE;
Keywords:
LACTOSYLCERAMIDE; MAC-1; NEUTROPHIL ADHESION; SUPEROXIDE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
34
Recensione:
Indirizzi per estratti:
Citazione:
T. Arai et al., "LACTOSYLCERAMIDE STIMULATES HUMAN NEUTROPHILS TO UP-REGULATE MAC-1, ADHERE TO ENDOTHELIUM, AND GENERATE REACTIVE OXYGEN METABOLITES IN-VITRO", Circulation research, 82(5), 1998, pp. 540-547

Abstract

Glycosphingolipids (GSLs) and their metabolites play important roles in a variety of biological processes. Wie have previously reported that lactosylceramide (LacCer), a ubiquitous GSL, stimulates NADPH oxidase-dependent superoxide generation by aortic smooth muscle cells and their consequent proliferation. We postulated that LacCer slay upregulate adhesion molecules on human polymorphonuclear leukocytes (hPMNs), perhaps also via NADPH oxidase-dependent reactive oxygen metabolite (ROM) generation, Incubation of hPMNs with LacCer upregulated CD11b/CD18 (Mac-1) and CD11c/CD18, as determined by fluorescence-automated cell sorting. LacCer also stimulated these hPMNs to generate superoxide via NADPH oxidase, as determined by lucigenin-enhanced chemiluminescence. However, the upregulation of Mac-1 by LacCer did not itself appear to be mediated by ROMs, since neither an antioxidant nor an NADPH oxidase inhibitor substantially inhibited the Mac-1 upregulation. However, this Mac-1 upregulation was significantly inhibited by two disparate phospholipase A(2) (PLA(2)) inhibitors. Moreover, LacCer induced arachidonic acid metabolism, which was inhibited by the PLA(2) inhibitors, bur nor by an NADPH oxidase inhibitor. To evaluate the effect of LacCer onhPMN adhesion to endothelium, hPMNs stimulated with LacCer were allowed to adhere to unstimulated human endothelial cell monolayers. LacCerstimulated hPMN adhesion to endothelial cells, which was blocked by anti-CD18 and by the PLA(2) inhibitors. We conclude that LacCer stimulates both Mac-1 upregulation and superoxide generation in hPMNs but that ROMs are not the upstream signal for Mac-1 upregulation. This mechanism may well be relevant to acute endothelial injury in inflammation and other pathological conditions.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/21 alle ore 07:59:45