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LFA-1/ICAM-3 mediates neutrophil homotypic aggregation under fluid shear stress (1996)

Okuyama, Masaki ; Kambayashi, Jun-ichi ; Sakon, Masato ; [et al.]

New York, N.Y. : Wiley-Blackwell

Journal of Cellular Biochemistry 60 (1996), S. 550-559

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ISSN: 0730-2312

Keywords: shear stress ; homotypic aggregation ; LFA-1 ; ICAM-3 ; NiCl2 sensitive Ca2+ channel ; Ca2+ influx ; Life and Medical Sciences ; Cell & Developmental Biology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Chemistry and Pharmacology , Medicine

Notes: We found that human neutrophils undergo homotypic aggregation by loading the physiological range of fluid shear stress (12-30 dynes/cm2). Under the fluid shear stress, an increase of intracellular Ca2+ concentration of neutrophils was observed. This increase of intracellular Ca2+ concentration was caused by Ca2+ influx, and the blockage of the flux by NiCl2 suppressed the neutrophil homotypic aggregation. Furthermore, this neutrophil aggregation under fluid shear stress was completely inhibited by pretreatment with antibody against LFA-1 or ICAM-3. These results suggested that NiCl2-sensitive Ca2+ channel played an important role in LFA-1/ICAM-3-mediated neutrophil homotypic aggregation under fluid shear stress. © 1996 Wiley-Liss, Inc.

Additional Material: 7 Ill.

Type of Medium: Electronic Resource

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