Transforming growth factor (TGF)- is implicated in fibrotic diseases, from various sources, such as pulmonary fibrosis and hepatic fibrosis. In nifedipine (NIF)- and phenytoin (PHT)-induced hyperplastic gingival tissues, significant immunostaining for TGF- is observed. TGF- is bifunctional, since it can either stimulate or inhibit the proliferation of fibroblasts derived from various sources. We have reported previously that PHT and NIF induce proliferation of cultured gingival fibroblasts, and that this is mediated by angiotensin II (Ang II). However, a possible role for TGF-1 in the proliferative response to Ang II has not been clarified. Therefore, we investigated the role of TNF- in the proliferative response of cultured r.at gingival fibroblasts (CRGF) to Ang II. NIF and Anf II enhanced the immunoreactivity of TGF- in CRGF. TGF-1 alone stimulated proliferation of CRGF as measured by MIT assay. Proliferation stimulated by Ang II was potentiated by TGF-1. The proliferation stimulated by TGF- and Ang II was inhibited by SB431542, a specific inhibitor of TGF-1 receptor kinase. These findings suggest tha TGF-1 enhances the proliferation of CRGF stimulated by Ang II.
P3-124
