title: Estrogen blocks parathyroid hormone-stimulated osteoclast-like cell formation in modulating differentiation of mouse marrow stromal cells in vitro.
abstract: OBJECTIVE
  During skeletal development and bone remodeling, bone marrow stromal cells give rise to osteoblasts and provide a critical microenvironment to support osteoclast formation. Estrogen is important for the maintenance of bone balance in adult animals by either increasing bone mass or inhibiting osteoclastic bone resorption. This study sought to determine the role that estrogen plays in coordinating osteogenic differentiation of bone marrow stromal cells and the ability of these cells to support osteoclast formation.
  
  
  METHODS
  A conditionally immortalized mouse bone marrow stromal cell line, MS1, was used to examine the effects of estrogen on stromal cell differentiation and on stromal cell-supported osteoclast formation.
  
  
  RESULTS
  On treatment of MS1 cells with 17 beta-estradiol (E2) (10(-12)-10(-8) M), alkaline phosphatase activity and bone nodule formation were increased in a dose-dependent manner, while the proliferation of MS1 cells was dose-dependently inhibited. 17 beta-E2 (10(-12)-10(-8) M) also caused a concentration-dependent inhibition of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cell (MNC) formation in parathyroid hormone (PTH)-stimulated MS1 and spleen cell cocultures. Furthermore, estrogen pretreatment of MS1 cells also decreased the number of TRAP-positive MNCs in cocultures. Culturing in PTH-treated conditioned media did not rescue the loss of activity supporting osteoclast-like cell formation in MS1 cells.
  
  
  CONCLUSIONS
  These results indicate that 17 beta-E2-stimulated osteoblastic differentiation of mouse marrow stromal cells results in bone matrix mineralization and a decrease in activity of supporting PTH-induced osteoclast-like cell formation.
authors.affiliation: School of Dentistry, College of Medicine, National Taiwan University.
authors.forename: Bu-Yuan
authors.initials: BY
authors.lastname: Liu
authors.forename: Pei-Wen
authors.initials: PW
authors.lastname: Wu
authors.forename: Yu-Ting
authors.initials: YT
authors.lastname: Hsu
authors.forename: Jiuan-Shin
authors.initials: JS
authors.lastname: Leu
authors.forename: Jeng-Tzung
authors.initials: JT
authors.lastname: Wang
mesh_terms: D000135:Acid Phosphatase / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001853:Bone Marrow / Q000502:physiology; D001854:Bone Marrow Cells / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D002454:Cell Differentiation / Q000187:drug effects*; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D018920:Coculture Techniques; D004305:Dose-Response Relationship, Drug; D004958:Estradiol / Q000494:pharmacology*; D007527:Isoenzymes / Q000378:metabolism; D051379:Mice; D010010:Osteoclasts / Q000502:physiology*; D010281:Parathyroid Hormone / Q000494:pharmacology*; D051381:Rats; D017154:Stromal Cells / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D000071681:Tartrate-Resistant Acid Phosphatase
chemical_list: D007527:Isoenzymes; D010281:Parathyroid Hormone; D004958:Estradiol; D000255:Adenosine Triphosphate; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase