Transforming growth factor type (3 (TGF-f3), when injected subcutaneously in newborn mice, causes formation of granulation tissue (induction of angiogenesis and activation offibroblasts to produce collagen) at the site of injection.These effects occur within 2-3 days at dose levels of <1 jg. Parallel in vitro studies show that TGF-(3 causes marked increase of either proline or leucine incorporation into collagen in either an NRK rat fibroblast cell line or early passage human dermal fibroblasts. Epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) do not cause these same in vivo and in vitro effects; in both rat and human fibroblast cultures, EGF antagonizes the effects of TGF-(3 on collagen formation. We have obtained further data to support a role for

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Abstract. Using immunohistochemical methods, we have investigated the role of transforming growth factor-13 (TGF-13) in the development of the mouse embryo. For detection of TGF-13 in ll-18-d-old embryos, we have used a polyclonal antibody specific for TGF-13 type 1 and the peroxidase-antiperoxidase technique. Staining of TGF-fl is closely associated with mesenchyme per se or with tissues derived from mesenchyme, such as connective tissue, cartilage, and bone. TGF-13 is conspicuous in tissues derived from neural crest mesenchyme, such as the palate, larynx, facial mesenchyme, nasal sinuses, meninges, and teeth. Staining of all of these tissues is greatest during periods of morphogenesis. In many instances, intense staining is seen in mesenchyme when critical interactions with adjacent epithelium occur, as in the development of hair follicles, teeth, and the submandibular gland. Marked staining is also seen when remodeling of mesenchyme or mesoderm occurs, as during formation of digits from limb buds, formation of the palate, and formation of the heart valves. The presence of TGF-13 is often coupled with pronounced angiogenic activity. The histochemical results are discussed in terms of the known biochemical actions of TGF-13, especially its ability to control both synthesis and degradation of both structural and adhesion molecules of the extracellular matrix.

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