Inhibition of angiogenesis in lipodermatosclerosis: Implication for venous ulcer formation

  • Authors:
    • Yared Herouy
    • Sebastian Kreis
    • Tobias Mueller
    • Thorsten Duerk
    • Georg Martiny-Baron
    • Petra Reusch
    • Florian May
    • Marco Idzko
    • Johannes Norgauer
  • View Affiliations

  • Published online on: November 1, 2009     https://doi.org/10.3892/ijmm_00000275
  • Pages: 645-651
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Abstract

Lipodermatosclerosis refers to skin induration of the lower extremities characterized by tortous, hyperpermeable vessels preceding venous leg ulcerations. Protein ligands and receptor tyrosine kinases that specifically regulate endothelial cell function are mainly involved in physiological as well as in disease-related angiogenesis. These ligand/receptor systems include the vascular endothelial growth factor (VEGF) and the angiopoietin (Ang) families and their receptor the tyrosine kinase with immunoglobulin-like domains (Tie-2) as well as the VEGF receptor family (VEGF-R1 and VEGF-R2). In the present study, the contribution of these endothelium-specific ligand/receptor systems in tissue samples of lipodermatosclerosis was evaluated. Our results provide evidence, that the mRNA-transcripts of VEGF (p<0.01), Ang-1 (p<0.1), Ang-2 (p<0.1) and VEGF-R1 (p<0.01) were significantly upregulated in all samples of lipodermatosclerosis in comparison with healthy skin by using reverse transcriptase-polymerase chain reaction. On protein level VEGF (p<0.01), Ang-1 (p<0.1), Ang-2 (p<0.1) and VEGF-R1 (p<0.01) were significantly elevated as well. Solely for Tie-2 and for VEGF-R2 no statistical difference could be detected on mRNA and protein level in patients with lipodermatosclerosis in comparison with healthy skin. By immunohistochemistry we confirmed upregulated protein expression for VEGF, Ang-1, Ang-2 and VEGF-R1 compared with healthy skin. Our findings strongly suggest that an imbalance between these ligand/receptor systems might contribute to the pathophysiology of advanced stages of chronic venous insufficiency. Inhibition of angiogenesis could significantly impact the tissue breakdown in lipodermatosclerosis and could hereby enable the formation of venous leg ulcerations.

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November 2009
Volume 24 Issue 5

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Herouy Y, Kreis S, Mueller T, Duerk T, Martiny-Baron G, Reusch P, May F, Idzko M and Norgauer J: Inhibition of angiogenesis in lipodermatosclerosis: Implication for venous ulcer formation. Int J Mol Med 24: 645-651, 2009.
APA
Herouy, Y., Kreis, S., Mueller, T., Duerk, T., Martiny-Baron, G., Reusch, P. ... Norgauer, J. (2009). Inhibition of angiogenesis in lipodermatosclerosis: Implication for venous ulcer formation. International Journal of Molecular Medicine, 24, 645-651. https://doi.org/10.3892/ijmm_00000275
MLA
Herouy, Y., Kreis, S., Mueller, T., Duerk, T., Martiny-Baron, G., Reusch, P., May, F., Idzko, M., Norgauer, J."Inhibition of angiogenesis in lipodermatosclerosis: Implication for venous ulcer formation". International Journal of Molecular Medicine 24.5 (2009): 645-651.
Chicago
Herouy, Y., Kreis, S., Mueller, T., Duerk, T., Martiny-Baron, G., Reusch, P., May, F., Idzko, M., Norgauer, J."Inhibition of angiogenesis in lipodermatosclerosis: Implication for venous ulcer formation". International Journal of Molecular Medicine 24, no. 5 (2009): 645-651. https://doi.org/10.3892/ijmm_00000275