Expression of 11β-hydroxysteroid dehydrogenase type 2 in lymphoblastic cells and its relationship with glucocorticoid sensitivity / 中国实验血液学杂志
Journal of Experimental Hematology
;
(6): 109-113, 2011.
Article
Dans Chinois
| WPRIM
| ID: wpr-244974
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.
Texte intégral:
Disponible
Indice:
WPRIM (Pacifique occidental)
Sujet Principal:
Pharmacologie
/
Lymphocytes
/
Cellules Jurkat
/
Lignée cellulaire tumorale
/
11-beta-Hydroxysteroid dehydrogenase type 2
/
Glucocorticoïdes
/
Énoxolone
/
Métabolisme
Type d'étude:
Etude diagnostique
Limites du sujet:
Humains
langue:
Chinois
Texte intégral:
Journal of Experimental Hematology
Année:
2011
Type:
Article
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