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Bone marrow cells are targets for the anabolic actions of prostaglandin E 2 on bone: Induction of a transition from nonadherent to adherent osteoblast precursors
Author(s) -
Scutt Andrew,
Bertram Petrina
Publication year - 1995
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1002/jbmr.5650100320
Subject(s) - prostaglandin e2 , osteocalcin , anabolism , alkaline phosphatase , osteoblast , bone marrow , mesenchymal stem cell , population , endocrinology , chemistry , in vitro , medicine , prostaglandin , matrix (chemical analysis) , microbiology and biotechnology , biology , biochemistry , enzyme , environmental health , chromatography
Although prostaglandin E 2 (PGE 2 ) is known to stimulate bone formation in vivo, its mechanism of action is not well understood. Circumstantial evidence suggests that bone marrow cells (BMC) may well be involved in this, and in order to investigate this further we have studied the effect of PGE 2 on proliferation and matrix synthesis in high‐density BMC cultures and on colony‐forming unit (CFU‐f) formation efficiency by BMC in vitro. High‐density cultures of BMC formed a collagenous, calcified matrix, synthesized osteocalcin and expressed alkaline phosphatase activity. The addition of PGE 2 caused a concentration‐dependent increase in total (but not specific) APase activity, cell number, and collagen accumulation. It was found that PGE 2 need only be present during the first 48 hours of the culture period and that longer exposure had no additional effect PGE 2 also caused a concentration‐dependent increase in CFU‐f formation, and it was found that this was due to the recruitment of new mesenchymal precursor cells from the nonadherent fraction of the BMC. Once again, the presence of PGE 2 for only the first 48 hours of the culture period was enough to precipitate a maximal response. We conclude that one mechanism for the anabolic actions of PGE 2 may be the recruitment of OB precursors from a population of nonadherent mesenchymal precursor cells present in the bone marrow.