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Prostaglandin e 2 promotes osteoclast formation in murine hematopoietic cultures through an action on hematopoietic cells
Author(s) -
Collins D.A.,
Chambers T.J.
Publication year - 1992
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.5650070512
Subject(s) - haematopoiesis , osteoclast , prostaglandin e2 , prostaglandin , cancer research , hematopoietic cell , action (physics) , microbiology and biotechnology , immunology , medicine , biology , stem cell , receptor , physics , quantum mechanics
Osteoclastic differentiation is induced from hematopoietic cells in the presence of 1,25‐(OH) 2 D 3 by stromal cells that are present in bone but not in hematopoietic spleen. Recent evidence suggests that prostaglandins (PGs) are essential for this process. In this communication we describe experiments in which we have examined further the role of PGE 2 in osteoclast formation. We found a marked reduction in basal, 1,25‐(OH) 2 D 3 , and IL‐3‐induced production of calcitonin receptor (CTR)‐positive cells and bone resorption by cyclooxygenase inhibitors, which was restored by PGE 2 addition. Although some stromal cell types (ST2 cells) that support osteoclast formation from spleen cells produced PGs in response to 1,25‐(OH) 2 D 3 , others (ts8 and calvarial cells) did not, either alone or in combination with spleen cells. On the other hand, both bone marrow and spleen cells produced amounts of PGE 2 in response to 1,25‐(OH) 2 D 3 that were sufficient to account for osteoclast formation. Osteoclast‐inductive ts8 cells were able to support osteoclast formation from spleen cells in the presence of 1,25‐(OH) 2 D 3 or PGE 2 even if devitalized. Incubation of ts8 cells in these agents before devitalization did not avoid the requirement for the presence of PGE 2 or 1,25‐(OH) 2 D 3 during subsequent incubation with spleen cells. Thus, hematopoietic cells produce sufficient PGE 2 for osteoclast formation, and the PGE 2 thus produced acts on hematopoietic precursors, which can be induced in the presence of PGE 2 to express CTR and resorb bone on contact with osteoclast‐inductive stromal cells. The ability of osteoclast‐inductive cells to support osteoclast formation appears not to rest on their ability to produce, induce, or respond to PGE 2 .