Expression of glucocorticoid receptor mRNAs in glucocorticoid-resistant nasal polyps

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 cau...

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Published inExperimental & molecular medicine pp. 466 - 473
Main Authors 최보라, 권재환, 공수정, 권민상, 조중환, 김재현, 오상택, 노환정, 김동은
Format Journal Article
LanguageKorean
Published 생화학분자생물학회 01.10.2006
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ISSN1226-3613
2092-6413

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Summary: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 (hGRα) and/or excessive presence of a GC receptor isoform, hGRβ 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 hGRα and hGRβ in nasal tissues. hGRα mRNA was more expressed in patients with nasal polyps than in normal subjects. However, the elevated hGRα mRNA expression was decreased after GC treatment. Compared with hGRα mRNA expression, level of hGRβ mRNA expression was very low in all groups. In patients, hGRβ 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 hGRβ mRNA. Thus, persistent GC-resistance is not associated with low expression of hGRα or overexpression of hGRβ. KCI Citation Count: 19
Bibliography:http://kmbase.medric.or.kr/Main.aspx?d=KMBASE&m=VIEW&i=0620920060380050466
G704-000088.2006.38.5.007
ISSN:1226-3613
2092-6413