Localization of transforming growth factor beta isoforms TGF-beta 1, TGF-beta 2, and TGF-beta 3 in surgically induced endometriosis in the rat.

Abstract

To elucidate the presence and cellular distribution of transforming growth factor beta (TGF-beta) in surgically induced endometriosis in the rat. Endometriosis was induced by implanting pieces of uterine fragments in the mesenteric region adjacent to a blood vessel for a period of 4-6 weeks. The endometrial implants were removed and processed for immunohistochemical localization using isoform-specific polyclonal antibodies to TGF-beta 1, TGF-beta 2, and TGF-beta 3. All the cell types in the endometrial implants with the exception of stromal cells immunostained for TGF-beta 1 and TGF-beta 3, but not TGF-beta 2. The inflammatory cells that were infiltrated among endometriotic stromal cells and implant-associated cysts contained the highest immunostaining intensity for TGF-beta s 1-3, followed by luminal and glandular epithelial cells, fibroblasts of the fibrous adhesions, and endothelial and smooth-muscle cells of arterioles. The immunostaining intensity of TGF-beta 1 was substantially higher than that of TGF-beta 3 and TGF-beta 2, and intensity was similar to the endometrial tissue from cycling rats in diestrus II for TGF-beta 1 and estrus for TGF-beta 2 and TGF-beta 3. In the cycling rats, the order of immunostaining intensity in the endometrium was TGF-beta 1, TGF-beta 3, and TGF-beta 2, respectively, with a higher intensity in diestrus II and proestrus than in diestrus I and estrus. The results indicate that endometrial implants in surgically induced endometriosis contain immunoreactive TGF-beta s, which may imply a possible paracrine/autocrine role for the action of TGF-beta in the maintenance of viable endometriotic tissue and the development of fibrous adhesions associated with the implants.