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Continuously applied compressive pressure induces bone resorption by a mechanism involving prostaglandin E 2 synthesis
Author(s) -
Imamura Kazunobu,
Ozawa Hiroyuki,
Hiraide Takatoshi,
Shibasaki Yoshinobu,
Fukuhara Tatsuo,
Takahashi Naoyuki,
Suda Tatsuo
Publication year - 1990
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041440207
Subject(s) - bone resorption , calvaria , chemistry , calcitonin , prostaglandin e , osteoblast , resorption , prostaglandin , prostaglandin e2 , endocrinology , osteoclast , medicine , acid phosphatase , andrology , receptor , biochemistry , biology , in vitro , enzyme
In previous research, we devised a specific culture chamber to examine the effect of continuously applied compressive pressure (CCP) on bone formation and resorption. The chamber was infused with compressed mixed gases with different O 2 and CO 2 composition to maintain the pO 2 , pCO 2 , and pH in the culture medium under pressures of +0.5 atm (1.5 atm total) to +2.0 atm (3.0 atm total) at the same levels as those at the ordinary pressure (1 atm). Using the specific culture chamber, we demonstrated that CCP greatly suppressed the differentiation of mouse osteoblast‐like MC3T3‐E1 cells. The inhibition by CCP appeared to be mediated by prostaglandin E 2 (PGE 2 ). In the present study, we examined the effect of CCP on osteoclastic bone resorption. CCP treatment of mouse bone marrow culture markedly increased both the PGE 2 production and the number of tartrateresistant acid phosphatase (TRACP)‐positive mononuclear cells (possibly precursors of multinucleated osteoclasts). An autoradiographic study using [ 125 l]‐salmon calcitonin showed clearly that those TRACP‐positive cells had calcitonin receptors. The CCP effect was the greatest at + 1.0 atm (2.0 atm total). Isobutylmethylxanthine potentiated the production of TRACP‐positive cells induced by CCP. Adding indomethacin completely inhibited both the TRACP‐positive cell formation and the PGE 2 production induced by CCP. CCP also increased the release of 45 Ca from prelabeled mouse calvaria during later stages (2–6 days) of the 6‐day culture period. CCP markedly increased PGE 2 but not interleukin 1 in the culture media of mouse calvaria. These results indicate that, besides inhibiting osteoblast differentiation, CCP stimulates bone resorption by generating new osteoclasts through a mechanism involving PGE 2 production.