2
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Plasma level and tissue expression of angiogenic factors in patients with hereditary hemorrhagic telangiectasia.

      Read this article at

      ScienceOpenPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The value of angiogenic factors interleukin-8 (IL-8) and vascular endothelial growth factor (VEGF) was determined in patients with hereditary hemorrhagic telangiectasia (HHT) to evaluate their role in HHT pathogenesis. IL-8 and VEGF were measured in plasma of 41 HHT patients and healthy controls by ELISA technique. In both groups, the IL-8 and VEGF tissue expression in cryostat sections of the nasal mucosa were then compared. VEGF plasma levels were significantly increased in HHT patients compared to healthy controls. In contrast, the IL-8 plasma levels in both groups did not show any significant difference. Compared to healthy controls, HHT tissue samples showed a weak IL-8 staining, whereas the VEGF staining was very strong. The plasma levels of VEGF and IL-8 could not be correlated to the patients' clinicopathological findings. Additionally to the angiogenic pro-inflammatory cytokine IL-8, the angiogenic factor VEGF seems to play a major role in HHT pathogenesis.

          Related collections

          Author and article information

          Journal
          Int. J. Mol. Med.
          International journal of molecular medicine
          1107-3756
          1107-3756
          Apr 2005
          : 15
          : 4
          Affiliations
          [1 ] Department of Otolaryngology, Head and Neck Surgery, University Hospital Mannheim, Theodor-Kutzer-Ufer, D-68135 Mannheim, Germany. haneen.sadick@hno.ma.uni-heidelberg.de
          Article
          15754019
          82d7a2d0-19c2-4dad-99af-4ae0e6b3becb
          History

          Comments

          Comment on this article