M. Morioka et al., Effect of interleukin-1 beta on aromatase activity and cell proliferation in human osteoblast-like cells (HOS), BIOC BIOP R, 268(1), 2000, pp. 60-64
Citations number
30
Categorie Soggetti
Biochemistry & Biophysics
Journal title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Osteoblast cells have a capacity to produce estrogen from androgen. Pt is k
nown that inflammatory cytokines in bone increase during estrogen deficienc
y. In the present study, the effect of interleukin-1 beta (IL-1 beta) on ar
omatase (Arom) activity in human osteoblast-like cells (HOS) was investigat
ed. We also investigated the effect of IL-1 beta and estradiol (E2) on cell
proliferation in NOS. [H-3] water method was employed to measure Arom acti
vity. Expression of Arom mRNA was determined by the reverse-transcription p
olymerase chain reaction (RT-PCR) method. The PCR products were confirmed b
y Southern blot analysis. Cell proliferation was measured by an ELISA-bromo
deoxyuridine (BrdU) kit. Addition of IL-1 beta increased Arom activity in
a dose-dependent manner and addition of IL-1 beta (10 ng/ml) resulted in 40
% greater activity than control. Addition of 500 ng/ml of human recombinant
IL-1 receptor antagonist neutralized the increased Arom activity to contro
l level. Stimulation of Arom mRNA expression by IL-1 beta was also found. I
L-1 beta and E2 stimulate osteoblastic cell proliferation significantly. Th
ese findings suggest for the first time that IL-1 beta stimulates Arom acti
vity through the IL-1 receptor and also cell proliferation in osteoblast-li
ke cells. It is also demonstrated that this stimulatory effect may be throu
gh the IL-1 receptor. Cell proliferation stimulated by IL-1 beta was reduce
d by the addition of the Arom inhibitor fadrozole-HCL (CGS-16949A). These r
esults imply that IL-1 beta has a stimulatory effect on estrogen formation
and sequentially cell proliferation in bone, and this mechanism may play an
important role in osteoblastic function especially in postmenopausal women
. (C) 2000 Academic Press.