title: Expression of adhesion molecules LFA-I and ICAM-I on osteoclast precursors during osteoclast differentiation and involvement of estrogen deficiency.
abstract: OBJECTIVE
  Estrogen deficiency caused by the menopause or ovariectomy leads to stimulation of osteoclastogenesis. The adhesion molecules, leukocyte function-associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1), are necessary for osteoclast formation. In this study, the expression of LFA-1 and ICAM-1 on osteoclast precursors during osteoclast differentiation, and the involvement of ovariectomy in the expression, were investigated.
  
  
  METHODS
  Spleen cells isolated from normal or ovariectomized (OVX) mice were co-cultured with TMS14, stromal cells derived from mouse bone marrow, in the absence or presence of 1 alpha,25-dihydroxyvitamin D3 (1 alpha,25(OH)2D3) for 7 days. On days 3, 5 and 7 of culture, the expression of LFA-1 and ICAM-1 on osteoclast precursors was quantitated using indirect immunofluorescence and confocal laser cytometry, and, on day 7, the number of formed osteoclasts was measured by tartrate-resistant acid phosphatase (TRAP) stain.
  
  
  RESULTS
  The level of ICAM-1 expression on osteoclast precursors gradually increased with osteoclast differentiation, whereas that of LFA-1 did not change. A high level of ICAM-1 was observed on the integrin beta 3-positive mononuclear cells. On the osteoclast precursors isolated from OVX mice, both the level of ICAM-1 expression per cell and the number of cells showing a high expression of ICAM-1 significantly increased, with an increase in the number of osteoclast-like cells. However, the level of LFA-1 did not change.
  
  
  CONCLUSIONS
  These results indicate that the expression level of ICAM-1, but not that of LFA-1, is involved in osteoclast differentiation. Estrogen deficiency results in an increase in ICAM-1 expression on osteoclast precursors, which may be one of the mechanisms underlying bone loss following the menopause or ovariectomy.
authors.affiliation: Department of Obstetrics and Gynecology, Faculty of Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Gao
authors.forename: I
authors.initials: I
authors.lastname: Morita
authors.forename: T
authors.initials: T
authors.lastname: Kubota
authors.forename: S
authors.initials: S
authors.lastname: Murota
authors.forename: T
authors.initials: T
authors.lastname: Aso
mesh_terms: D000135:Acid Phosphatase; D000818:Animals; D001854:Bone Marrow Cells / Q000166:cytology; D002455:Cell Division; D004958:Estradiol / Q000172:deficiency / Q000494:pharmacology; D005260:Female; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000187:drug effects / Q000378:metabolism*; D007527:Isoenzymes; D016169:Lymphocyte Function-Associated Antigen-1 / Q000378:metabolism*; D051379:Mice; D010010:Osteoclasts / Q000201:enzymology / Q000378:metabolism*; D010052:Ovariectomy; D013154:Spleen / Q000166:cytology; D000071681:Tartrate-Resistant Acid Phosphatase; D013997:Time Factors
chemical_list: D007527:Isoenzymes; D016169:Lymphocyte Function-Associated Antigen-1; D018799:Intercellular Adhesion Molecule-1; D004958:Estradiol; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase