Wound healing in hemophilia B mice and low tissue factor mice.

Journal Article (Journal Article;Review)

Wound healing involves a number of physiologic mechanisms including coagulation, inflammation, formation of granulation tissue, and tissue remodeling. Coagulation with robust thrombin generation leading to fibrin formation is necessary for wound healing. It is less clear if there is a requirement for ongoing coagulation to support tissue remodeling. We have studied wound healing in mice with defects in both the initiation (low tissue factor) and propagation (hemophilia B) phases. In hemophilia B mice, dermal wound healing is delayed; this delay is associated with bleeding into the granulation tissue. Mice can be treated with replacement therapy (factor IX) or bypassing agents (factor VIIa) to restore thrombin generation. If treated just prior to wound placement, mice will have normal hemostasis in the first day of wound healing. As the therapeutic agents clear, the mice will revert to hemophilic state. If the primary role of coagulation in wound healing is to provide a stable platelet/fibrin plug that is loaded with thrombin, then treating hemophilic animals just prior to wound placement should restore normal wound healing. The results from this study did not support that hypothesis. Instead the results show that restoring thrombin generation only at the time of wound placement did not improve the delayed wound healing. In preliminary studies on low tissue factor mice, there also appears to be a delay in wound healing with evidence of bleeding into the granulation tissue. The current data suggests that ongoing coagulation function needs to be maintained to support a normal wound healing process.

Full Text

Duke Authors

Cited Authors

  • Monroe, DM; Mackman, N; Hoffman, M

Published Date

  • April 2010

Published In

Volume / Issue

  • 125 Suppl 1 / Suppl 1

Start / End Page

  • S74 - S77

PubMed ID

  • 20170942

Pubmed Central ID

  • PMC2855851

Electronic International Standard Serial Number (EISSN)

  • 1879-2472

Digital Object Identifier (DOI)

  • 10.1016/j.thromres.2010.01.043


  • eng

Conference Location

  • United States