| First Author | Kulig E | Year | 1998 |
| Journal | Endocr Pathol | Volume | 9 |
| Issue | 3 | Pages | 261-274 |
| PubMed ID | 12114718 | Mgi Jnum | J:51465 |
| Mgi Id | MGI:1316794 | Doi | 10.1007/BF02739967 |
| Citation | Kulig E, et al. (1998) Remodeling of hyperplastic pituitaries in hypothyroid alpha-subunit knockout mice after thyroxine and 17 beta- estradiol treatment: Role of apoptosis. Endocr Pathol 9(3):261-274 |
| abstractText | Hyperplasia of pituitary thyrotrophs is often associated with hypothyroidism. In this study, the effects of thyroxine and 17 beta-estradiol on thyrotroph hyperplasia was analyzed using a hypothyroid mouse model resulting from targeted disruption of the glycoprotein hormone a- subunit (alpha SU) gene, which leads to lack of functional thyroid-stimulating hormone (TSH), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) and underdevelopment of the thyroid and gonads. Thyroxine replacement for 2 mo resulted in a decrease in the relative percent of thyrotrophs and an increase of lactotrophs and somatotrophs numbers to normal values. A twofold increase in the relative percent of gonadotrophs was observed compared to wild-type mouse pituitary. Treatment for 2 mo with 17 beta-estradiol led to an increase in lactotroph numbers to normal levels, but had no influence on thyrotroph hyperplasia. Rearrangement of the hyperplastic pituitary phenotype after hormonal replacement proceeded without any evidence of pituitary cell necrosis. A slight increase in apoptotic cell death was observed in hormone-treated pituitaries, and this was localized to TSH cells by double-labeling experiments. Chronic thyroxine treatment resulted in increased expression of Bcl-2 protein in hypertrophied pituitary cells, whereas 17 beta-estradiol increased expression of Bad protein in prolactin cells. These results suggest that apoptotic cell death is involved in reversal of thyrotroph hyperplasia in the presence of thyroid hormone. Thyroxine and 17 beta- estradiol may influence cell death in this model by regulating expression of the Bcl-2 protein family in a cell-type specific manner. |
