Sex hormones mediate interleukin-1 beta production by human osteoblastic HOBIT cells.
Sex hormones mediate interleukin-1 beta production by human osteoblastic HOBIT cells.
复制标题
性激素介导人成骨细胞 HOBIT 细胞产生白细胞介素 1 β。
DOI：
10.1016/0303-7207(95)03549-m
复制
发表时间：
1995
影响因子：
4.1
通讯作者：
Keeting,PE
中科院分区：
文献类型：
--
作者：
Pivirotto,LA;Cissel,DS;Keeting,PE
性激素实现其骨保护作用的机制仍然没有解决。白细胞介素-1 β（IL-1β）是一种自分泌/旁分泌的骨调节因子，可能以雌激素敏感的方式产生。在人成骨细胞HOBIT细胞模型中测试性腺类固醇对IL-1β产生的调节。用17β-雌二醇或睾酮处理6- 4 - 8 h后，IL-1β mRNA水平呈剂量依赖性增加4-8倍（P < 0.05）。这些反应的受体介导通过使用17α-雌二醇或氟替卡松的实验来指示。IL-1β mRNA水平的肿瘤坏死因子-α（TNF）依赖性增加与类固醇的作用相加。TNF和TNF可增加IL-1β蛋白的释放（P < 0.05），而17β-雌二醇对IL-1β蛋白的释放无明显影响。性腺类固醇的骨保护作用可能部分通过介导局部IL-1β产生来实现。
The mechanisms by which the sex hormones achieve their bone-sparing effects remains unresolved. Interleukin-1β (IL-1β) is an autocrine/paracrine regulator of bone that may be produced in an estrogen-sensitive manner. The regulation of IL-1β 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-1β mRNA levels followed a 6–48 h treatment with 17β-estradiol or testosterone. Receptor mediation of these responses was indicated by experiments using 17α-estradiol or flutamide. Tumor necrosis factor-α (TNF) dependent increases in IL-1β mRNA levels were additive to the effects of the steroids. Testosterone and TNF increased IL-1β protein release (P < 0.05) while 17β-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-1β production.