We have recently reported that transforming growth factor‐β stimulates genuine connective tissue repair in the perforated rat mesentery and that this stimulation is not caused by increased macrophage chemotaxis. To further characterize the effect of transforming growth factor‐β1on the enhanced rate of wound closure, we performed a series of morphometric analyses with determination of mitotic index, fibroblast labeling index, cellular density, neovascularization, and scar tissue formation. Actin expression close to the wound margin was also evaluated morphologically. Fibroblast cell proliferation was not stimulated by transforming growth factor‐β1in either wounded or unwounded tissue. Transforming growth factor‐β1did, however, significantly increase the formation of healing tissue postoperative days 5 to 10 (p<0.05) and angiogenesis was significantly stimulated by transforming growth factor‐β1postoperative days 7 and 10 (p<0.005). The mean cellular density was significantly increased in unperforated, transforming growth factor‐β1‐treated membranes from days 3 to 10, and increased expression of actin with time was observed close to the wound margin. Transforming growth factor‐β1was thus shown to be a potent stimulator of angiogenesis and healing tissue formation in connective tissue repair, but this stimulation mainly occurred after closure of perforations. The increased cellular density in the absence of stimulated proliferation and increased actin expression in wound cells indicate that contraction may be an important mechanism of connective tissue repair in the pe
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