Thromb Haemost 2005; 94(02): 432-437
DOI: 10.1160/TH05-04-0291
Wound Healing and Inflammation/Infection
Schattauer GmbH

Impaired wound healing in factor XIII deficient mice

Amir Inbal*
1  Institutes of Thrombosis and Hemostasis, Tel Aviv University, Israel
,
Aharon Lubetsky*
1  Institutes of Thrombosis and Hemostasis, Tel Aviv University, Israel
,
Tanya Krapp
1  Institutes of Thrombosis and Hemostasis, Tel Aviv University, Israel
,
David Caste
1  Institutes of Thrombosis and Hemostasis, Tel Aviv University, Israel
2  Institutes of Cardiology Research, Tel Aviv University, Israel
,
Aviv Shaish
3  Institutes of Lipid and Atherosclerosis Research, Sheba Medical Center, Tel Hashomer, and Sackler Faculty of Medicine, Tel Aviv University, Israel
,
Gerhardt Dickneitte
4  Pharmacology and Toxicology, ZLB-Behring, Marburg, Germany
,
Laszlo Modis
5  Department of Anatomy Histology and Embryology, University of Debrecen
,
Laszlo Muszbek
6  Medical and Health Science Center, Clinical Research Center and Thrombosis and Hemostasis Research Group of the Hungarian Academy of Sciences, University of Debrecen, Debrecen, Hungary
,
Aida Inbal
1  Institutes of Thrombosis and Hemostasis, Tel Aviv University, Israel
› Author Affiliations
Further Information

Publication History

Received: 27 April 2005

Accepted after major revision: 03 June 2005

Publication Date:
05 December 2017 (online)

Summary

Factor XIII that stabilizes fibrin clots in the final stages of blood coagulation also participates in wound healing,as can be inferred from a delay in wound repair in some patients with inherited FXIII deficiency. In this study we evaluated the effect of FXIII on wound healing in FXIII-deficient mice. Three groups of mice (n = 10) were employed: control group, FXIII-deficient group and FXIII-deficient group treated with FXIII concentrate. Excisional wounds were left unsutured and undressed, and mice were followed for eleven days. FXIII-deficient mice exhibited impaired wound healing as has been demonstrated by 15%, 27% and 27% decrease in percentage of wound closure on day 4, 8 and 11, respectively. On day 11 complete healing was observed in control (100% closure), 73.23% in FXIII-deficient and 90.06% in FXIII deficient/FXIII-treated groups (p = 0.007 by ANOVA and p = 0.001 by t-test between control and FXIII-deficient groups). Scoring system representing maturation rate of the wounds showed that the scores for the control,FXIII-deficient and FXIIIdeficient/ FXIII treated groups were 94.9 ± 4.7, 61.5 ± 14.5 and 94.5 ± 6.4, respectively (p < 0.001 by ANOVA). Histological analysis of the lesions performed at day 11 disclosed delayed reepithelization and necrotized fissure in FXIII-deficient mice and normal healing in FXIII-deficient/FXIII-treated mice. The findings of this study confirm that in FXIII-deficient mice wound healing is delayed and the cellular and tissue defects can be corrected by treatment with FXIII, providing evidence for the essential role of FXIII in wound repair and remodeling.

* First authors