Transforming growth factor beta(3) promotes fascial wound healing in a newanimal model

Hypothesis: Transforming growth factor beta(3) (TGF-beta(3)) promotes fasci al wound healing in a new animal model, as measured by wound breaking stren gth, collagen deposition, and cellular proliferation. Design/Intervention: Bilateral, longitudinal incisions were made in the ant erior rectus sheaths of 24 male New Zealand white rabbits. One incision was treated with 1 mu g of TGF-beta(3); the contralateral incision served as a control. The wounds were harvested at 1, 2, 3, 4, 6, and 8 weeks after cre ation ("wounding"). Main Outcome Measures: Wound tissue was tested for breaking strength using a tensiometer and processed for histological er;amination of collagen depos ition and cellular proliferation at all time points after wounding. Collage n deposition and cellular proliferation were measured in histological cross sections of wounds with Masson trichrome staining and proliferating cell n uclear antigen immunohistochemistry, respectively. Results: At all time points after wounding, treatment with TGF-beta(3) sign ificantly increased the wound breaking strength (up to 138%) and collagen d eposition (up to 150%) over the control group. Cellular proliferation was i ncreased during the first 3 weeks after wounding (up to 147%),but returned to baseline levels by the fourth week. Conclusions: Transforming growth factor beta(3) promotes fascial wound heal ing. In this new animal model of fascial wound healing, TGF-beta(3) increas ed fascia breaking strength, collagen deposition, and cellular proliferatio n. These results are similar to findings in cutaneous wound models and demo nstrate, for the first time, a pharmacologic agent to accelerate fascial he aling.