Regulation of 11β-hydroxysteroid dehydrogenase 1 and 2 by IGF-1 in mice

被引:12
作者
Huang, Yadong [2 ,3 ,4 ]
Li, Xingwang [1 ]
Lin, Han [1 ,4 ]
Chu, Yanhui [5 ]
Chen, Bingbing [6 ]
Lian, Qingquan [1 ]
Ge, Ren-Shan [1 ,4 ]
机构
[1] 2nd Affiliated Hosp, Wenzhou Med Coll, Wenzhou 325027, Zhejiang, Peoples R China
[2] Jinan Univ, Inst Life, Guangzhou 510632, Guangdong, Peoples R China
[3] Jinan Univ, Inst Hlth Engn, Guangzhou 510632, Guangdong, Peoples R China
[4] Populat Council, New York, NY 10065 USA
[5] Mudanjiang Med Univ, Heilongjiang Key Lab Antifibrosis Biotherapy, Mudanjiang, Heilongjiang, Peoples R China
[6] Wenzhou Med Coll, Sch Pharm, Wenzhou 325000, Zhejiang, Peoples R China
关键词
Corticosterone; 11 beta-Hydroxysteroid dehydrogenase; IGF-1; BETA-HYDROXYSTEROID DEHYDROGENASE; APPARENT MINERALOCORTICOID EXCESS; RAT LEYDIG-CELLS; GROWTH-HORMONE; GLUCOCORTICOID METABOLISM; IN-VIVO; MODULATION; EXPRESSION; CORTISONE; TYPE-1;
D O I
10.1016/j.bbrc.2009.12.148
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Two isoforms of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD1 and 11 beta-HSD2) play an important role in regulation of glucocorticoid corticosterone (CORT, the active form in rodents) by the interconversion between CORT and 11-dehydrocorticosterone (11DHC, the biologically inert form). 11 beta-HSD1 is an NADP+/NADPH-dependent oxidoreductase which is mainly expressed in liver and kidney, while 11 beta-HSD2 is an NAD+-dependent oxidase which is predominantly expressed in kidney. The regulation of 11 beta-HSD1 and 11 beta-HSD2 mRNA (Hsd11b1 and Hsd11b2) levels and their activities by IGF-1 was performed in liver, kidney, and testis of IGF-1 knockout mate mice. Real-time PCR showed that Hsd11b1 in liver was decreased while Hsd11b2 mRNA level was decreased in kidney of IGF-1 null mice. 11 beta-HSD1 and 11 beta-HSD2 activities fluctuated with the changes of their respective Hsd11b1 or Hsd11b2 mRNA levels. In conclusion, IGF-1 tissue-specifically regulates Hsd11b1 and Hsd11b2 expression. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:1752 / 1756
页数:5
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