[Expression of 11β-hydroxysteroid dehydrogenase type 2 in lymphoblastic cells and its relationship with glucocorticoid sensitivity]

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2011 Feb;19(1):109-13.
[Article in 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.

Publication types

  • English Abstract

MeSH terms

  • 11-beta-Hydroxysteroid Dehydrogenase Type 2 / metabolism*
  • Cell Line, Tumor
  • Glucocorticoids / pharmacology*
  • Glycyrrhetinic Acid / analogs & derivatives
  • Glycyrrhetinic Acid / pharmacology
  • Humans
  • Jurkat Cells
  • Lymphocytes / drug effects
  • Lymphocytes / metabolism*

Substances

  • Glucocorticoids
  • 18alpha-glycyrrhetinic acid
  • 11-beta-Hydroxysteroid Dehydrogenase Type 2
  • Glycyrrhetinic Acid