He Ping, Sun Gang
Department of Physiology, Second Military Medical University, Shanghai 200433, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2003 Aug;19(3):291-4.
To study the co-localization of glucocorticoid receptor and 11beta-hydroxysteroid dehydrogenase 1 (11beta-HSD1) and to investigate whether glucocorticoids regulate the reductase activity and expression of 11beta-HSD1.
Immunohistochemical staining for 11beta-HSD1 in cultured primary human chorionic trophoblasts was performed. Radiometric conversion assay and Northern blot analysis were respectively used to observe the activity and mRNA expression of 11beta-HSD1.
11beta-HSD1 and GR were co-expressed in the same chorionic trophoblast. Both 11beta-HSD1 reductase activity and mRNA levels were increased by dexamethasone (10(-6) mol/L, 10(-7) mol/L) in the cultured chorionic trophoblasts, and the effects were blocked by GR antagonist RU486 (10(-6) mol/L).
By binding to GR, glucocorticoids induce the expression of 11beta-HSD1 by a possible intracrine mechanism.
研究糖皮质激素受体与11β-羟基类固醇脱氢酶1(11β-HSD1)的共定位,并探讨糖皮质激素是否调节11β-HSD1的还原酶活性及表达。
对培养的原代人绒毛膜滋养层细胞进行11β-HSD1免疫组织化学染色。分别采用放射转化分析和Northern印迹分析观察11β-HSD1的活性及mRNA表达。
11β-HSD1和GR在同一绒毛膜滋养层细胞中共表达。地塞米松(10⁻⁶mol/L、10⁻⁷mol/L)可使培养的绒毛膜滋养层细胞中11β-HSD1还原酶活性及mRNA水平升高,且这些作用被GR拮抗剂RU486(10⁻⁶mol/L)阻断。
糖皮质激素通过与GR结合,可能以内分泌机制诱导11β-HSD1的表达。