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Mediators of Inflammation
Volume 2013 (2013), Article ID 219313, 10 pages
Research Article

Antiangiogenic VEGF Isoform in Inflammatory Myopathies

1Department of Medicine, Surgery and Neuroscience, University of Siena, Via A. Moro 2, 53100 Siena, Italy
2Department of Molecular and Developmental Medicine, University of Siena, Via A. Moro 2, 53100 Siena, Italy
3Child Neuropsychiatry Unit, University Hospital AOUS, Viale M. Bracci 16, 53100 Siena, Italy
4Department of Life Sciences and Biotechnologies, University of Ferrara, Via L. Borsari 46, 44121 Ferrara, Italy
5Department of Food and Nutrition, Kyung Hee University, Seoul 130-701, Republic of Korea

Received 12 March 2013; Revised 1 May 2013; Accepted 15 May 2013

Academic Editor: Jeffrey H. Ruth

Copyright © 2013 Nila Volpi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Objective. To investigate expression of vascular endothelial growth factor (VEGF) antiangiogenic isoform on human muscle in idiopathic inflammatory myopathies (IIM) and to compare distribution of angiogenic/antiangiogenic VEGFs, as isoforms shifts are described in other autoimmune disorders. Subjects and Methods. We analyzed and VEGF-A by western blot and immunohistochemistry on skeletal muscle biopsies from 21 patients affected with IIM (polymyositis, dermatomyositis, and inclusion body myositis) and 6 control muscle samples. TGF-β, a prominent VEGF inductor, was analogously evaluated. Intergroup differences of western blot bands density were statistically examined. Endomysial vascularization, inflammatory score, and muscle regeneration, as pathological parameters of IIM, were quantitatively determined and their levels were confronted with VEGF expression. Results. was significantly upregulated in IIM, as well as TGF-β. VEGF-A was diffusely expressed on unaffected myofibers, whereas regenerating/atrophic myofibres strongly reacted for both VEGF-A isoforms. Most inflammatory cells and endomysial vessels expressed both isoforms. levels were in positive correlation to inflammatory score, endomysial vascularization, and TGF-β. Conclusions. Our findings indicate skeletal muscle expression of antiangiogenic and preferential upregulation in IIM, suggesting that modulation of VEGF-A isoforms may occur in myositides.