Neutralisation of uPA with a monoclonal antibody reduces plasmin formation and delays skin wound healing in tPA-deficient mice

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

  • Annika Jögi
  • Birgitte Rønø
  • Ida K Lund
  • Boye S Nielsen
  • Michael Ploug
  • Gunilla Høyer-Hansen
  • John Rømer
  • Leif R Lund
Proteolytic degradation by plasmin and metalloproteinases is essential for epidermal regeneration in skin wound healing. Plasminogen deficient mice have severely delayed wound closure as have mice simultaneously lacking the two plasminogen activators, urokinase-type plasminogen activator (uPA) and tissue-type plasminogen activator (tPA). In contrast, individual genetic deficiencies in either uPA or tPA lead to wound healing kinetics with no or only slightly delayed closure of skin wounds.
TidsskriftP L o S One
Udgave nummer9
Sider (fra-til)e12746
StatusUdgivet - 1 sep. 2010

ID: 33752700