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LFA‐1/ICAM‐3 mediates neutrophil homotypic aggregation under fluid shear stress
Author(s) -
Okuyama Masaki,
Kambayashi Junichi,
Sakon Masato,
Monden Morito
Publication year - 1996
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/(sici)1097-4644(19960315)60:4<550::aid-jcb11>3.0.co;2-l
Subject(s) - intracellular , icam 1 , shear stress , chemistry , biophysics , biology , biochemistry , materials science , composite material
We found that human neutrophils undergo homotypic aggregation by loading the physiological range of fluid shear stress (12–30 dynes/cm 2 ). Under the fluid shear stress, an increase of intracellular Ca 2+ concentration of neutrophils was observed. This increase of intracellular Ca 2+ concentration was caused by Ca 2+ influx, and the blockage of the flux by NiCl 2 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 NiCl 2 ‐sensitive Ca 2+ channel played an important role in LFA‐1/ICAM‐3‐mediated neutrophil homotypic aggregation under fluid shear stress. © 1996 Wiley‐Liss, Inc.