gms | German Medical Science

43. Kongress der Deutschen Gesellschaft für Rheumatologie, 29. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie, 25. Wissenschaftliche Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie

02.-05. September 2015, Bremen

Pathomechanisms in dermatomyositis and polymyositis: role of endothelial progenitor cells

Meeting Abstract

  • Dana Burghardt - Universitätsmedizin Göttingen, Klinik für Nephrologie und Rheumatologie, Göttingen
  • Jens Schmidt - Universitätsmedizin Göttingen, Klinik für Neurologie, Göttingen
  • Arne Wrede - Universitätsmedizin Göttingen, Göttingen
  • Boris Lemmer - Universität Göttingen, Göttingen
  • Katrin Schwarze - Universitätsmedizin Göttingen, Göttingen
  • Daniel Patschan - Universitätsklinikum Göttingen, Nephrologie und Rheumatologie, Göttingen
  • Gerhard A. Müller - Klinik für Nephrologie und Rheumatologie Universitätsmedizin Göttingen, Göttingen
  • Susann Patschan - Universitätsklinikum Göttingen, Nephrologie und Rheumatologie, Göttingen

Deutsche Gesellschaft für Rheumatologie. Deutsche Gesellschaft für Orthopädische Rheumatologie. Gesellschaft für Kinder- und Jugendrheumatologie. 43. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh); 29. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh); 25. wissenschaftliche Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR). Bremen, 02.-05.09.2015. Düsseldorf: German Medical Science GMS Publishing House; 2015. DocER.15

doi: 10.3205/15dgrh069, urn:nbn:de:0183-15dgrh0697

Published: September 1, 2015

© 2015 Burghardt et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at



Introduction: The pathogenesis of dermatomyositis (DM) is believed to rely on humoral mechanisms, whereas the hypothesized cause of polymyositis (PM) are cytotoxic T cells. Presuming that cells of the immune system immigrate from small vessels of the affected muscle, significant endothelial dysfunction may be present in both diseases. Moreover, vessels in DM have been shown to become massively destructed. Endothelial progenitor cells (EPCs) are required for neovascularization upon ischemic damage. Aim of this project was to analyze the presence and functional alteration of EPCs in DM, PM, and healthy controls.

Methods: Twenty-five patients (DM 15, PM 10) and 23 healthy controls were included into the study. The following EPC-related parameters were evaluated: blood-derived EPC colonies (culture assay) and peripheral circulating EPCs (CD133+/KDR+ cells - cytometric analysis). Muscle biopsies were available from 9 patients with DM and from 8 with PM. Cryosections from muscle biopsies were stained with markers for CD31 (endothelium), Nestin (regeneration of mature endothelial cells), MHC (inflammation) and CXCR6 (T-lymphocyte receptor for tissue recruitement) and evaluated by immunofluorescence followed by manual multi-parameter assessment.

Results: Blood-derived EPC colonies were significantly lower in PM as compared to healthy controls, the difference between the latter and DM was only close to the level of significance. Staining of musclebiopsies revealed strong signals for MHC-I and Nestin. The marker of endothelial regeneration Nestin showed an even more positive trend in both PM and DM as compared to CXCR6 and MHC-I.

Conclusion: The data suggest that (I) impairement of the EPC system may perpetuate vascular damage in DM / PM. (II) Higher abundances of intramuscular nestin suggest that mature endothelial cells ´attempt´ to endogenously neutralize affected EPC competence.