Increased Expression of Glucocorticoid Receptor beta Messenger RNA in Patients with Ankylosing Spondylitis.
10.3904/kjim.2005.20.2.146
- Author:
Chang Keun LEE
1
;
Eun Young LEE
;
You Sook CHO
;
Keun Ae MOON
;
Bin YOO
;
Hee Bom MOON
Author Information
1. Division of Allergy and Rheumatology, Department of Internal Medicine, Asan Institute for Life Science, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. cklee@amc.seoul.kr
- Publication Type:Original Article ; Comparative Study ; Research Support, Non-U.S. Gov't
- Keywords:
Ankylosing Spondylitis;
Glucocorticoid Receptor;
Rheumatoid Arthritis
- MeSH:
Adult;
Comparative Study;
Female;
*Gene Expression;
Genetic Markers;
Humans;
Leukocytes, Mononuclear/metabolism;
Male;
Middle Aged;
RNA, Messenger/biosynthesis/*genetics;
Receptors, Glucocorticoid/biosynthesis/*genetics;
Research Support, Non-U.S. Gov't;
Retrospective Studies;
Reverse Transcriptase Polymerase Chain Reaction;
Spondylitis, Ankylosing/*blood/genetics
- From:The Korean Journal of Internal Medicine
2005;20(2):146-151
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Glucocorticoids have been known to be less effective for treating ankylosing spondylitis (AS) patients than for treating rheumatoid arthritis (RA) patients. To elucidate the mechanisms underlying this phenomenon, we evaluated whether the glucocorticoid receptor (GR) beta expression of the peripheral blood mononuclear cells (PBMCs) in patients with AS is increased compared with patients with RA. METHODS: PBMCs were isolated from the subjects of 3 study groups: the healthy controls (n=25), the RA patients (n=25), and the AS patients (n=25). All the subjects had never taken corticosteroids and the patients with RA or AS were newly diagnosed. The expression of GR beta messenger RNA (mRNA) was determined by reverse transcription of the total RNA, and this was followed by semi-quantitative polymerase chain reaction analysis (RT-PCR). RESULTS: The level of GR alpha mRNA expression was not different among three groups. GR beta mRNA expression of the AS patients (2.02 [range: 0.99-7.21], median [25th-75th percentiles]) was enhanced compared with that of the controls (0.78 [range: 0.43-1.62]) and the RA patients (0.98 [range: 0.79-1.18]). The level of GR beta mRNA expression was not related to the inflammatory markers or the disease activity score 28 for the RA patients, and it was not related to the Bath ankylosing spondylitis disease activity index for the AS patients. CONCLUSION: The expression of GR beta mRNA, which is a dominant negative regulator for the glucocorticoid response, was increased in AS patients. The results suggest that the increased expression of GR beta mRNA may be related to the ineffectiveness of glucocorticoids for the treatment of AS.
