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Bone‐resorbing activity of thyroid hormones is related to prostaglandin production in cultured neonatal mouse calvaria
Author(s) -
Klaushofer Klaus,
Hoffmann Oskar,
Gleispach Helmut,
Leis HansJörg,
Czerwenka Erwin,
Koller Kristian,
Peterlik Meinrad
Publication year - 1989
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.5650040304
Subject(s) - calvaria , endocrinology , medicine , hormone , prostaglandin e2 , thyroid hormones , prostaglandin , thyroid , prostaglandin e , biology , in vitro , biochemistry
The bone‐resorbing activity of thyroid hormones was evaluated in neonatal mouse calvaria maintained in organ culture for 96 h. Thyroxine (T 4 ) between 10 −8 and 10 −5 mol/liter and triiodothyronine (T 3 ) between 10 −8 and 10 −7 mol/liter caused a dose‐dependent release of calcium from cultured bone. The thyroid hormone effect was delayed in onset for at least 24 h, and after 96 h of culture amounted to 50–90% of the bone‐resorbing activity of 10 −8 mol/liter parathyroid hormone (PTH). The bone‐resorbing action of T 4 as well as of T 3 was completely blocked by 100 U/ml interferon‐γ (IF‐ γ ) or 20 mU/ml salmon calcitonin (CT). “Escape” from CT inhibition, which is a well‐known phenomenon in the action of PTH, was not observed with thyroid hormone‐mediated bone resorption. Thyroid hormone treatment of cultured calvaria resulted in a gradual increase between 48 and 96 h of medium concentrations of prostaglandin (PG) E 2 and particularly of 6‐keto‐PGF 1α , the inactive metabolite of prostacyclin (PGI 2 ). The release of PGF 2α in general was not significantly affected. Although the effect of thyroid hormones on PG release from cultured calvaria was completely abolished by 5 × 10 −7 mol/liter indomethacin, in some experiments indomethacin reduced thyroid hormone‐mediated bone resorption by only 50%. This indicates that thyroid hormone action on bone is also mediated by a PG‐independent mechanism.