Sex hormones mediate interleukin-1 beta production by human osteoblastic HOBIT cells.
The mechanisms by which the sex hormones achieve their bone-sparing effects remains unresolved. Interleukin-1 beta (IL-1 beta) is an autocrine/paracrine regulator of bone that may be produced in an estrogen-sensitive manner. The regulation of IL-1 beta production by the gonadal steroids was tested in the human osteoblastic HOBIT cell model. Dose-dependent 4-8-fold increases (P < 0.05) in IL-1 beta mRNA levels followed a 6-48 h treatment with 17 beta-estradiol or testosterone. Receptor mediation of these responses was indicated by experiments using 17 alpha-estradiol or flutamide. Tumor necrosis factor-alpha (TNF) dependent increase IL-1 beta mRNA levels were additive to the effects of the steroids. Testosterone and TNF increased IL-1 beta protein release (P < 0.05) while 17 beta-estradiol had little effect on release. The bone-sparing effects of the gonadal steroids may be accomplished, in part, through their mediation of local IL-1 beta production.
Pivirotto
L A
LA
Department of Biology, West Virginia University, Morgantown 26505-6057, USA.
Cissel
D S
DS
Keeting
P E
PE
D002460:Cell Line; D004958:Estradiol / Q000494:pharmacology; D005485:Flutamide / Q000494:pharmacology; D012739:Gonadal Steroid Hormones / Q000494:pharmacology*; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis* / Q000235:genetics; D010006:Osteoblasts / Q000187:drug effects / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D013739:Testosterone / Q000037:antagonists & inhibitors / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
D012739:Gonadal Steroid Hormones; D007375:Interleukin-1; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D013739:Testosterone; D004958:Estradiol; D005485:Flutamide