Glucocorticoid receptor variants may predispose to rheumatoid arthritis susceptibility
| dc.contributor.author | Chatzikyriakidou, A. | en |
| dc.contributor.author | Georgiou, I. | en |
| dc.contributor.author | Voulgari, P. V. | en |
| dc.contributor.author | Georgiadis, A. N. | en |
| dc.contributor.author | Argyriou, E. | en |
| dc.contributor.author | Drosos, A. A. | en |
| dc.date.accessioned | 2015-11-24T19:14:41Z | |
| dc.date.available | 2015-11-24T19:14:41Z | |
| dc.identifier.issn | 0300-9742 | - |
| dc.identifier.uri | https://olympias.lib.uoi.gr/jspui/handle/123456789/21367 | |
| dc.rights | Default Licence | - |
| dc.subject | genetic-basis | en |
| dc.subject | resistance | en |
| dc.subject | polymorphisms | en |
| dc.subject | sensitivity | en |
| dc.subject | mechanisms | en |
| dc.subject | mutation | en |
| dc.title | Glucocorticoid receptor variants may predispose to rheumatoid arthritis susceptibility | en |
| heal.abstract | Objectives: Deregulation of glucocorticoid (GC) secretion could be associated with rheumatoid arthritis (RA). The GC receptor (GR) has two isoforms. In the present study, we explored the role of GR- polymorphisms rs33388, rs33389, and Bcl I, and the GR- variant rs6198 in RA susceptibility. Methods: One hundred and thirty-six RA patients and 148 ethnic matching controls were studied. Polymorphisms rs33388 and Bcl I were genotyped by polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP), and variants rs33389 and rs6198 by polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) coupled with sequencing. Arlequin and SPSS softwares were used in the statistical analysis. Results: The polymorphisms studied were in Hardy-Weinberg equilibrium in both groups. A marginally statistical significant difference was observed in the distribution of rs33388 genotypes between RA patients and controls (p=0.053). When the A and T alleles were compared, the statistical significance was p=0.025. Specific complex genotypes were also differentially distributed: the GR- complex genotypes (a) [homozygote (homo) wild-type (wt) rs33388-homo wt rs33389] (11% RA vs. 21% controls; p=0.023), (b) [homo wt rs33388-homo wt rs33389-homo non-wt Bcl I] (0.7% RA vs. 4.7% controls; p=0.042), and (c) the GR- complex genotype [homo wt rs33388-homo wt rs33389-homo non-wt Bcl I-homo wt rs6198] (0.7% RA vs. 4.7% controls; p=0.042). Conclusions: GR- and GR- polymorphisms are potentially associated with RA susceptibility. However, additional studies in larger and other ethnic groups of patients are needed to confirm the results of the present study. | en |
| heal.access | campus | - |
| heal.fullTextAvailability | TRUE | - |
| heal.identifier.primary | 10.1080/03009740802366068 | - |
| heal.identifier.secondary | <Go to ISI>://WOS:000263093900001 | - |
| heal.identifier.secondary | http://informahealthcare.com/doi/abs/10.1080/03009740802366068 | - |
| heal.journalName | Scandinavian Journal of Rheumatology | en |
| heal.journalType | peer-reviewed | - |
| heal.language | en | - |
| heal.publicationDate | 2009 | - |
| heal.recordProvider | Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής | el |
| heal.type | journalArticle | - |
| heal.type.el | Άρθρο Περιοδικού | el |
| heal.type.en | Journal article | en |
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