title: [Cell surface adhesion molecules mediated stretch-induced HL-60 cell adhesion to mouse common carotid arteries].
abstract: OBJECTIVE
  To compare the roles of vascular cell adhesion molecular-1 (VCAM-1) and P-selectin in stretch-induced HL-60 cell adhesion to mouse common carotid arteries.
  
  
  METHODS
  After the isolated mouse common carotid arteries were perfused with HL-60 cells, the unbound leukocytes were washed away and the number of adherent cells in every single field was counted under a microscope. We first observed the effect of stretch on HL-60 cell adhesion to the endothelium of arteries under different magnitudes of luminal hydrostatic pressure. Then, the roles of VCAM-1 and P-selectin in stretch-induced HL-60 cell adhesion to mouse common carotid arteries were compared by the pretreatment of neutralizing antibodies against VCAM-1, P-selectin or isotype-matched control antibody, respectively.
  
  
  RESULTS
  The increase in luminal hydrostatic pressure of carotid arteries led to the increase of the number of HL-60 adhesion cells, suggesting that stretch induced HL-60 cell adhesion in a magnitude-dependent manner. The pretreatment with the isotype-matched control antibody failed to induce a significant change of the number of HL-60 adhesion cells. In contrast, the pretreatment of both VCAM-1 and P-selectin neutralizing antibodies dramatically reduced the number of adherent leukocytes (P<0.05), although no statistical significance was observed between the two groups.
  
  
  CONCLUSIONS
  Stretch can induce HL-60 cell adhesion to carotid arteries in a magnitude-dependent manner. VCAM-1 and P-selectin play some roles in mechanical stretch-induced HL-60 cell adhesion to mouse common carotid arteries.
authors.affiliation: Laboratory of Vascular Biology, Institute of Molecular Medicine, Peking University, Beijing 100871, China.
authors.forename: Yingqing
authors.initials: Y
authors.lastname: Huo
authors.affiliation: Laboratory of Vascular Biology, Institute of Molecular Medicine, Peking University, Beijing 100871, China.
authors.forename: Beibei
authors.initials: B
authors.lastname: Jiang
authors.affiliation: Laboratory of Vascular Biology, Institute of Molecular Medicine, Peking University, Beijing 100871, China.
authors.forename: Xiaofan
authors.initials: X
authors.lastname: Han
authors.affiliation: Laboratory of Vascular Biology, Institute of Molecular Medicine, Peking University, Beijing 100871, China.
authors.forename: Jincai
authors.initials: J
authors.lastname: Luo
mesh_terms: D000818:Animals; D057134:Antibodies, Neutralizing / Q000276:immunology / Q000494:pharmacology; D017536:Carotid Artery, Common / Q000276:immunology / Q000378:metabolism*; D002448:Cell Adhesion / Q000187:drug effects; D004730:Endothelium, Vascular / Q000276:immunology / Q000378:metabolism*; D018922:HL-60 Cells; D006801:Humans; D006874:Hydrostatic Pressure; D051379:Mice; D019007:P-Selectin / Q000378:metabolism*; D013314:Stress, Mechanical; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism*
chemical_list: D057134:Antibodies, Neutralizing; D019007:P-Selectin; D019010:Vascular Cell Adhesion Molecule-1