title: Expression of messenger RNA for transforming growth factor-beta1 and for transforming growth factor-beta receptors in peripheral blood of systemic lupus erythematosus patients treated with low doses of quinagolide.
abstract: The objective of this study was to determine the expression of transforming growth factor-beta1 messenger RNA (TGF-beta1 mRNA) and the expression of mRNA for TGF-beta receptors (TGF-beta Rs mRNA) in whole peripheral blood of consecutive (treated from several months to several years) systemic lupus erythematosus (SLE) patients (21 women). A further aim of this study was to evaluate the association between expression of the above mentioned parameters in relation to the form of applied therapy (9 patients treated with quinagolide and 12 with quinagolide plus prednisone, azathioprine or cyclosporine A). The control group consisted of 15 healthy women. Most of the patients had mild SLE with SLE disease activity index (SLEDAI) score < 10 at time when blood samples were collected. Laboratory measurements included real-time polymerase chain reaction (RT-QPCR). The expression levels of TGF-beta1 mRNA and mRNA for TGF-beta RII and RIII were significantly lower in patients whereas the expression level of TGF-beta RI was statistically significantly higher in SLE patients than in the controls. A very high positive correlation between TGF-beta1 mRNA expression and expression levels of TGF-beta Rs mRNA was found. In compared subgroups selected according to the form of the applied therapy no statistically significant differences were observed. We conclude that the TGF-beta signaling pathway can be altered in circulating leukocytes derived from treated patients with SLE and that the assumed forms of the applied therapy in the group of patients under consideration are accompanied by similarity in the expression level of transcripts for TGF-beta1 and TGF-beta Rs determined in whole blood. In our investigations, we cannot exclude the influence of the disease itself on the obtained results.
authors.affiliation: Department of Internal, Autoimmune and Metabolic Diseases, Medical University of Silesia, ul Medyków 14, Katowice, Poland. genmar@ka.onet.pl
authors.forename: Antoni
authors.initials: A
authors.lastname: Hrycek
authors.forename: Dariusz
authors.initials: D
authors.lastname: Kusmierz
authors.forename: Tomasz
authors.initials: T
authors.lastname: Dybała
authors.forename: Longina
authors.initials: L
authors.lastname: Swiatkowska
mesh_terms: D000293:Adolescent; D000328:Adult; D000634:Aminoquinolines / Q000627:therapeutic use*; D001379:Azathioprine / Q000627:therapeutic use; D016572:Cyclosporine / Q000627:therapeutic use; D018491:Dopamine Agonists / Q000627:therapeutic use*; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000188:drug therapy* / Q000235:genetics / Q000276:immunology; D008875:Middle Aged; D011241:Prednisone / Q000627:therapeutic use; D012333:RNA, Messenger / Q000096:biosynthesis* / Q000235:genetics; D018125:Receptors, Transforming Growth Factor beta / Q000096:biosynthesis / Q000235:genetics* / Q000276:immunology; D053773:Transforming Growth Factor beta1 / Q000096:biosynthesis / Q000235:genetics* / Q000276:immunology
chemical_list: D000634:Aminoquinolines; D018491:Dopamine Agonists; D012333:RNA, Messenger; D018125:Receptors, Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; C046650:quinagolide; D016572:Cyclosporine; D001379:Azathioprine; D011241:Prednisone