Urotensin-II in systemic sclerosis: a new peptide in pathogenesis


Pehlivan Y., Onat A. M. , Comez G., Babacan T.

CLINICAL RHEUMATOLOGY, vol.30, no.6, pp.837-842, 2011 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 30 Issue: 6
  • Publication Date: 2011
  • Doi Number: 10.1007/s10067-011-1688-3
  • Journal Name: CLINICAL RHEUMATOLOGY
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.837-842
  • Bursa Uludag University Affiliated: No

Abstract

Systemic sclerosis (SSc) is a rare multisystem chronic disease and its etiology is still unknown. To obtain and generate reasonable treatment methods, new mediators or targets are needed. Urotensin-II (U-II) is predominantly a vasoactive peptide with fibrotic and prothrombotic features. Like endothelin-1 (ET-1), U-II could play an important role in SSc pathogenesis given its properties of convenient one-to-one SSc pathogenetic pathways. A consecutive group of 55 patients diagnosed with SSc and 30 healthy controls were included in the study. Patients and healthy controls were evaluated for clinical and laboratory manifestations, specific organ involvement, autoantibodies, and activity scores specific for SSc. In addition, plasma ET-1 and plasma levels of U-II-like immunoreactivity of both groups were compared. ET-1 level significantly increased in the SSc group in contrast to the healthy controls (6.38 +/- 1.39 and 0.99 +/- 0.27 pg/ml; p = 0.006). U-II was also significantly elevated in patients, and the plasma levels of U-II-like immunoreactivity were positively correlated with ET-1 (8.19 +/- 1.74 and 1.02 +/- 0.19 pg/ml; p = 0.003 and p = 0.0001; r = 0.887). For reasonable treatment of SSc, we need to focus on new targets such as ET-1 and U-II. This study hypothesized that these mediators could have a role in SSc pathogenesis, and U-II antagonist might be a potential alternative therapy for these patients.