Exp Mol Med.
2006 Oct;38(5):466-473.
Expression of glucocorticoid receptor mRNAs in glucocorticoid-resistant nasal polyps
- Affiliations
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- 1Department of Biotechnology and Bioengineering, and Biomaterial Control Dong-Eui University, Busan, Korea. kimde@deu.ac.kr
- 2Department of Otorhinolaryngology-Head and Neck Surgery, Maryknoll General Hospital, Busan, Korea.
- 3Nambu Blood Laboratory, Korean Red Cross, Busan, Korea.
- 4PharmcoGenomics Research Center, Inje University, Busan, Korea.
- 5Department of Otolaryngology, College of Medicine, Pusan National University, Busan, Korea.
Abstract
- Glucocorticoids (GCs) are the most effective group of medications available to treat inflammation. Although most patients with inflammation respond to GC, a small group of patients exhibit persistent GC-resistance with prolonged inflammation. Previously, it was proposed that the GC-resistance is caused by low amount of human GC receptor (hGR alpha) and/or excessive presence of a GC receptor isoform, hGR beta that was generated from alternative splicing of the hGR message. We have tested this hypothesis by investigating correlation between the expression pattern of hGR mRNAs in patients with inflammatory nasal polyps and the effectiveness of GC treatment.? We have performed reverse transcription PCR analysis of mRNAs coding each hGR alpha and hGR beta in nasal tissues.? hGR alpha mRNA was more expressed in patients with nasal polyps than in normal subjects. However, the elevated hGR alpha mRNA expression was decreased after GC treatment. Compared with hGR alpha mRNA expression, level of hGR beta mRNA expression was very low in all groups. In patients, hGR beta mRNA was expressed at a similar level regardless of GC efficacy, indicating that there is no correlation between the GC sensitivity and the expression level of hGR beta mRNA. Thus, persistent GC-resistance is not associated with low expression of hGRa or over- expression of hGR beta.
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