Effects of Thyroid Hormone on Preduction of Interleukin-6 and Interleukin-11 in Human Bone Marrow Stromal Cells.
- Author:
Chul Hee KIM
;
Dong Kwan KIM
;
Hong Kyu KIM
;
Young Ki SONG
;
Ki Soo KIM
- Publication Type:Original Article
- Keywords:
Thyroid hormone;
Osteoporosis;
Bone marrow stromal cells;
Interleukin-6;
Interleukin-l1;
Interleukin-l;
Estradiol
- MeSH:
Bone Marrow*;
Bone Resorption;
Estradiol;
Estrogens;
Humans*;
Interleukin-1;
Interleukin-11*;
Interleukin-6*;
Mesenchymal Stromal Cells*;
Metabolism;
Osteoblasts;
Osteoclasts;
Osteoporosis;
Stromal Cells;
Thyroid Gland*;
Thyroid Hormones
- From:Journal of Korean Society of Endocrinology
1997;12(4):557-564
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: It is well known that excessive thyroid hormone in the body is associated with bone loss. However, the mechanism by which thyroid hormone affects bone cell metabolism remains unclear. It has been shown that thyroid hormones stimulate osteoclastic bone resorption indirectly via some unknown mediators secreted by osteoblasts, This study was undertaken to determine if interleukin-6 (IL-6) or interleukin-11 (IL-l1) could be the mediator (s) of thyroid hormone-induced bone loss. METHODS: We treated primary cultured human bone rnarrow stromal cells with 3,5,3-triiodo-thyronine (T) and measured basal and interleukin-l (IL-1)-stimulated IL-6/IL-ll production. We also investigated the possible modulating effect of 17B-estradiol (17B-E2.) on thyroid hormone action. RESULTS: T3 at 10 (-12) ~ 10 (-8) M concentration, significantly increased the basal IL-6 production in a dose-dependent manner, and also potentiated the stimulatory effect of IL-1 on IL-6 production. However, T failed to elicit a detectable effect on basal or IL-1-stimulated IL-11 production. Treat#ment with l7B-E2. inhibited IL-1-stimulated IL-6 production, but the effects of T3 on IL-6 production were not affected by 17/B-E. CONCLUSION: These results suggest that thyroid hormone may increase bone resorption by increasing basal IL-6 production and potentiating IL-1-induced IL-6 production from osteoblast-lineage cells, and these effects were independent of estrogen status.
