Expression of 11β-hydroxysteroid dehydrogenase type 2 in lymphoblastic cells and its relationship with glucocorticoid sensitivity.
- Author:
Yi TAO
1
;
Ju-Mei SHI
;
Yan-Xiang ZHANG
;
Lu GAO
;
Feng-Huang ZHAN
Author Information
1. Department of Hematology, Shanghai Tenth People Hospital, Tongji University School of Medicine, Shanghai 200072, China.
- Publication Type:Journal Article
- MeSH:
11-beta-Hydroxysteroid Dehydrogenase Type 2;
metabolism;
Cell Line, Tumor;
Glucocorticoids;
pharmacology;
Glycyrrhetinic Acid;
analogs & derivatives;
pharmacology;
Humans;
Jurkat Cells;
Lymphocytes;
drug effects;
metabolism
- From:
Journal of Experimental Hematology
2011;19(1):109-113
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to explore the expression of 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) in 3 different lymphoblastic cell lines with relation to their glucocorticoid (GC) sensitivity. The 11β-HSD2 expressions in acute lymphoblastic leukemia Jurkat cells, lymphoma Daudi and Raji cells, and peripheral blood T cells of a healthy volunteer were analyzed by real time PCR and Western blot. Glucocorticoid (GC)-induced apoptosis in 3 different cell lines was detected by flow cytometry. Cell growth in Jurkat cells treated with cortisol was analyzed by trypan blue dye exclusion. Flow cytometry was performed to observe GC-induced apoptosis in Jurkat cells treated by combination of GC with 11β-HSD2 inhibition 18β-glycyrrhetinic acid (18β-GA). The results demonstrated that 11β-HSD2 highly expressed in Jurkat cells, but not in Daudi, Raji cells and normal blood T cells. Compared to Daudi and Raji cells, Jurkat cells were more resistant to GC-induced apoptosis. Furthermore, the inhibition of 11β-HSD2 by 18β-GA resulted in increased cellular sensitivity to GC as shown by elevated induction of apoptosis. it is concluded that 11β-HSD2 is at least partly responsible for GC resistance in Jurkat cells. 11β-HSD2 may be a potential target for reduction of GC-resistance in therapeutic applications.
