Adrenomedullin induces lymphangiogenesis and ameliorates secondary lymphoedema.

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  • Author(s): Jin D;Jin D; Harada K; Ohnishi S; Yamahara K; Kangawa K; Nagaya N
  • Source:
    Cardiovascular research [Cardiovasc Res] 2008 Dec 01; Vol. 80 (3), pp. 339-45. Date of Electronic Publication: 2008 Aug 16.
  • Publication Type:
    Journal Article; Research Support, Non-U.S. Gov't
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Oxford Journals Country of Publication: England NLM ID: 0077427 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1755-3245 (Electronic) Linking ISSN: 00086363 NLM ISO Abbreviation: Cardiovasc Res Subsets: MEDLINE
    • Publication Information:
      Publication: 2008- : Oxford : Oxford Journals
      Original Publication: London, British Medical Assn.
    • Subject Terms:
      Adrenomedullin/*physiology ; Lymphangiogenesis/*physiology ; Lymphedema/*physiopathology; Animals ; Cell Movement ; Cell Proliferation ; Cells, Cultured ; Cyclic AMP/physiology ; Disease Models, Animal ; Endothelium, Lymphatic/cytology ; Endothelium, Lymphatic/physiology ; Extracellular Signal-Regulated MAP Kinases/physiology ; Humans ; Lymphedema/drug therapy ; Male ; Mice ; Mice, Inbred BALB C ; Mitogen-Activated Protein Kinase Kinases/physiology ; Neovascularization, Physiologic/physiology ; Signal Transduction/physiology ; Vasodilation/physiology
    • Abstract:
      Aims: Adrenomedullin (AM) is a multifunctional peptide hormone that plays a significant role in vasodilation and angiogenesis. Lymphoedema is a common but refractory disorder that is difficult to be treated with conventional therapy. We therefore investigated whether AM promotes lymphangiogenesis and improves lymphoedema.
      Methods and Results: The effects of AM on lymphatic endothelial cells (LEC) were investigated. AM promoted proliferation, migration, and network formation of cultured human lymphatic microvascular endothelial cells (HLMVEC). AM increased intracellular cyclic adenosine monophosphate (cAMP) level in HLMVEC. The cell proliferation induced by AM was inhibited by a cAMP antagonist and mitogen-activated protein kinase kinase (MEK) inhibitors. Phosphorylated extracellular signal-regulated kinase (ERK) in HLMVEC was increased by AM. Continuous administration of AM (0.05 microg/kg/min) to BALB/c mice with tail lymphoedema resulted in a decrease in lymphoedema thickness. AM treatment increased the number of lymphatic vessels and blood vessels in the injury site.
      Conclusion: AM promoted LEC proliferation at least in part through the cAMP/MEK/ERK pathway, and infusion of AM induced lymphangiogenesis and improved lymphoedema in mice.
    • Comments:
      Comment in: Cardiovasc Res. 2008 Dec 1;80(3):324-5. (PMID: 18835842)
    • Accession Number:
      148498-78-6 (Adrenomedullin)
      E0399OZS9N (Cyclic AMP)
      EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
      EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
    • Publication Date:
      Date Created: 20080819 Date Completed: 20090310 Latest Revision: 20131121
    • Publication Date:
      20231215
    • Accession Number:
      10.1093/cvr/cvn228
    • Accession Number:
      18708640