Effect of oestradiol on cytokine production in immortalized human marrow stromal cell lines.
Effect of oestradiol on cytokine production in immortalized human marrow stromal cell lines.
复制标题
雌二醇对永生化人骨髓基质细胞系细胞因子产生的影响。
DOI:
10.1006/cyto.2001.0956
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发表时间:
2001
期刊:
影响因子:
3.8
通讯作者:
M. Cohen
中科院分区:
文献类型:
--
作者:
A. C. Ramalho;A. Jullienne;P. Couttet;A. Graulet;C. Morieux;M. de Vernejoul;M. Cohen
Oestrogen deficiency enhances bone osteoclastogenesis and bone resorption. Evidence of cooperation between stromal cells and osteoclast precursors in mice suggests that oestradiol acts by regulating cytokine release from stromal cells. Bone marrow stroma contains multipotent progenitors that give rise to many mesenchymal lineages, including osteoblasts that may regulate osteoclast differentiation. We immortalized and characterized six human bone marrow stromal cell lines (presence of Stro1, secretion of alkaline phosphatase, osteocalcin, formation of lipid droplets, and presence of alpha and beta oestrogen receptors). The response of cytokines to oestradiol was then evaluated in vitro, as were the phorbol myristate acetate (PMA)-stimulated cytokine levels. Cells had the characteristics of undifferentiated stromal cells (Stro1+, RANK-L+), and expressed alpha-oestrogen receptors. The osteoblast phenotype (amounts of alkaline phosphatase and osteocalcin) was weak and there was a poor capacity to differentiate into adipocytes. These cell lines did not respond to oestradiol by producing interleukin 6 (IL-6), IL-1 or tumour necrosis factor alpha (TNF-alpha) either constitutively or after stimulation with PMA. Moreover, RANK-L and osteoprotegerin expressions were not regulated by oestradiol in vitro. Thus, modulation of these cytokines by stromal cells do not appear to be the mechanism by which oestradiol regulates bone resorption in humans.
影响因子:
4.8
作者:
Passeri,G;Girasole,G;Jilka,RL;Manolagas,SC
通讯作者:
Manolagas,SC
影响因子:
4.8
作者:
L. Hofbauer;S. Khosla;C. Dunstan;D. Lacey;T. Spelsberg;B. Riggs
通讯作者:
L. Hofbauer;S. Khosla;C. Dunstan;D. Lacey;T. Spelsberg;B. Riggs