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Amir Inbal, ÁOK VIInstitute of Thrombosis and Hemostasis, Sheba Medical Center, Tel Hashomer,Israel and Clinical Research Center, Medical and Health Science Center,University of DebrecenIMPAIRED HEALING OF CUTANEOUS WOUNDS IN FACTOR XIII-DEFICIENT MICEBlood coagulation factor XIII (FXIII) is a heterotetramer composed oftwo A (the potentially active enzyme) and two B (carrier protein) subunits.Activated FXIII stabilizes fibrin clots at the final stages of blood coagulation bycross-linking glutamine and lysine residues of fibrin chains. FXIII participates intissue remodeling, wound healing, as can be inferred from defects in theseprocesses in patients with inherited FXIII deficiency. Wound healing andembryo implantation are complex processes involving cell proliferation andangiogenesis. Recently, we have demonstrated using in vitro and in vivo modelsthat FXIII promotes angiogenesis. Since angiogenesis is vital for wound healingwe evaluated the effect of factor XIII on wound healing in FXIII-deficient mice.Three mice groups each containing 10 mice was employed: control group,FXIII-deficient group and FXIII-deficient group treated intraperitonially withFXIII concentrate - Fibrogammin-P (ZLB-Behring, Germany). Excisionalwounds were inflicted by a full-thickness 3-mm disposable punch biopsy. Allwounds were left unsutured and undressed, and mice were followed for elevendays. FXIII-deficient mice exhibited impaired wound healing as has beendemonstrated by 15%, 5% and 19% decrease in percentage of wound closure atday 4, 8 and 11, respectively. At day 11 complete healing was observed incontrol (100% closure), 81.4% in FXIII-deficient and 96.32% in FXIIIdeficient/FXIIItreated groups (p < 0.05 by ANOVA and p < 0.05 by t-testbetween control and FXIII-deficient groups). Scoring system representingmaturation of the wounds as a function of time was implemented. The scores forthe control, FXIII-deficient and FXIII-deficient/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 delayedreepithelization by keratinocytes, impaired concentration of fibroblasts in thedermal layer and necrotized fissure at the wound site in FXIII-deficient mice.The findings of this study confirm that in FXIII-deficient mice wound healing isdelayed and the cellular and tissue defects can be corrected by treatment withFXIII, providing a substantial evidence for the essential role of FXIII in woundrepair and remodeling.Témavezető: Prof.Dr. Aida Inbal, Prof.Dr. László Muszbek