A549 기도 상피세포에서 GRβ의 과발현이 스테로이드에 의한 전체 유전자 변화에 미치는 영향

Background: Glucocorticoid receptor β (GRβ) may not bind to ligands and is thought to affect gene transcription only by acting as a dominant negative inhibitor of Glucocorticoid receptor α (GRα). However, there have been few reports about the functional roles of GRβ in the steroid-induces changes of...

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Published inChʻŏnsik mit alrerugi Vol. 28; no. 3; pp. 220 - 225
Main Authors 이호연, Ho Youn Lee, 김남희, Nam Hee Kim, 김도형, Doh Hyung Kim, 김윤섭, Youn Seop Kim, 박재석, Jae Seuk Park, 김동훈, Dong Hoon Kim, 지영구, Young Koo Jee
Format Journal Article
LanguageKorean
Published 대한천식알레르기학회 30.09.2008
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Summary:Background: Glucocorticoid receptor β (GRβ) may not bind to ligands and is thought to affect gene transcription only by acting as a dominant negative inhibitor of Glucocorticoid receptor α (GRα). However, there have been few reports about the functional roles of GRβ in the steroid-induces changes of gene expression. Objective: To investigate the functional role of GRβ overexpression in the steroid-induced changes of gene expression. Method: The changes in gene expressions such as steroid-induced synthesis of genes, TNF-α-induced synthesis of inflammatory genes and steroid induced suppression of activated genes by TNF-α treatment were compared with and without pCMV GRβ expression. Result: The number of genes increased by dexamethasone treatment only in the GRβ transfected group were 54. Increased expressions of genes by dexamethasone treatment were not affected by GRβ overexpression. The number genes increased by TNF-α treatment only in the GRβ-transfected group were 69. Expressions of genes increased by TNF-α treatment in both the control and the GRβ-transfected group were decreased by further dexamethasone treatment in a similar manner. Conclusion: The results of this study suggest that GRβ may not be a dominant negative inhibitor in the steroid-induced changes of genes and that it may have some functional roles in the regulation of gene expressions. (Korean J Asthma Allergy Clin Immunol 2008;28: 220-225)
Bibliography:The Official Publication of the Korean Society of Allergology
G704-000986.2008.28.3.006
ISSN:1226-8739