COLVα2 a Biomarker of Vasculopathy in Scleroderma?
Jymenez Morais, Patricia Martin, Isabele C Camargo, Maria L Katayama, Solange Carrasco, Claudia Goldeinstein-Schainberg, Edwin R Parras, Fernanda Barrence, Ana P Velosa, Vera L Capelozzi, Walcy R Teodora. University of São Paulo Medical School, São Paulo, Brazil; Institute of Biomedical Sciences of the University of São Paulo, São Paulo, Brazil
Background: The type V collagen (COLV) mutations are involved in collagen vascular diseases, such as systemic sclerosis (SSc), in which an unusual accumulation of this collagen was demonstrated in this disesase. Immunogenic properties, histoarchitecture differentiated and changes in mRNA expression COLV may suggest that such modifications, assigned to this protein may be correlated with disease pathogenesis.
Design: Our aim in this study was evaluate COLVα1 and COLVα2 expression in skin scleroderma patients. Skin biopsies of 9 patients and 12 controls were obtained from SSc according American College of Rheumatology (CAPPesq 0817/07, CAPPesq 0436/08). The qualitative analyze of COLVα1 and COLVα2 was performed by confocal microscopy and immunofluorescence. Confirmation of results will be made gene expression this chains, associate immunogold analysis.
Results: The COLVα2 immunostained showed distorted and strongly thickened fibers in skin with irregular bundles of COLVα2 distributed in parallel and perpendicular arrangements. These distributions resulting in a dense network around of the vessels in SSc patients compared with thin fibers pattern from the healthy controls. In contrast COLVα1 expression was absent in superficial derma compared with respective controls. The immunogold analysis to COLVα1 and COLVα2 confirmed the immunofluorescence and quantitative molecular evaluation demonstrated an increase of COLVα2 gene expression in SSc skin when compared to control (p= 0.05).
Conclusions: The overexpression of COLVα2 fibers, besides the biochemical changes,suggest an interference with the fibrillogenesis process in skin fibrosis from SSc patients, reinforcing the participation of this protein collagen in pathogenesis of SSc.
Wednesday, March 6, 2013 9:30 AM
Poster Session V # 302, Wednesday Morning