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首页> 外文期刊>Journal of cellular biochemistry. >Specific induction of heat shock protein 27 by glucocorticoid in osteoblasts.
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Specific induction of heat shock protein 27 by glucocorticoid in osteoblasts.

机译：糖皮质激素在成骨细胞中特异性诱导热休克蛋白27。

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摘要

It is generally recognized that osteoporosis is a common complication of patients with glucocorticoid excess and that glucocorticoid receptor is associated with heat shock protein (HSP) 70 and HSP90 in a heterocomplex. In the present study, we investigated whether glucocorticoid induces HSP27, HSP70, and HSP90 in osteoblast-like MC3T3-E1 cells. Dexamethasone time-dependently increased the levels of HSP27, while having no effect on the levels of HSP70 or HSP90. The effect of dexamethasone was dose-dependent in the range between 0.1 nM and 0.1 microM. Dexamethasone induced an increase of the levels of mRNA for HSP27. Dexamethasone induced the phosphorylation of p38 mitogen-activated protein (MAP) kinase. SB203580 and PD169316, inhibitors of p38 MAP kinase, suppressed the HSP27 accumulation by dexamethasone. In addition, SB203580 reduced the dexamethasone-stimulated increase of the mRNA levels for HSP27. The dexamethasone-induced phosphorylation of p38 MAP kinase was reduced by SB203580. These results strongly suggest that glucocorticoid stimulates the induction of neither HSP70 nor HSP90, but HSP27 in osteoblasts, and that p38 MAP kinase is involved in the induction of HSP27.
机译：通常认为，骨质疏松是糖皮质激素过多患者的常见并发症，并且糖皮质激素受体与异源复合物中的热休克蛋白（HSP）70和HSP90相关。在本研究中，我们调查了糖皮质激素是否在成骨细胞样MC3T3-E1细胞中诱导HSP27，HSP70和HSP90。地塞米松随时间增加了HSP27的水平，而对HSP70或HSP90的水平没有影响。地塞米松的作用在0.1 nM和0.1 microM之间是剂量依赖性的。地塞米松诱导HSP27 mRNA水平升高。地塞米松诱导p38丝裂原活化蛋白（MAP）激酶的磷酸化。 p38 MAP激酶抑制剂SB203580和PD169316抑制了地塞米松对HSP27的积聚。另外，SB203580减少了地塞米松刺激的HSP27 mRNA水平的增加。 SB203580降低了地塞米松诱导的p38 MAP激酶的磷酸化。这些结果强烈提示糖皮质激素既不刺激成骨细胞中的HSP70也不刺激HSP90，而是刺激HSP27，并且p38 MAP激酶参与了HSP27的诱导。

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