Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P10415 (Bcl-2)
 33,771 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperplasia of pituitary thyrotrophs is often associated with hypothyroidism. In this study. the effects of thyroxine and 1 7B-estradiol on thyrotroph hyperplasia was analyzed using a hypothyroid mouse model resulting from targeted disruption of the glycoprotein hormone a-subunit (aSU) 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 17B-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 17f3-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-estradiol may influence cell death in this model by regulating expression of the Bcl-2 protein family in a celltype specific manner.
 ...
PMID:Remodeling of Hyperplastic Pituitaries in Hypothyroid us-Subunit Knockout Mice After Thyroxine and 1713-Estradiol Treatment: Role of Apoptosis. 1211 18

Zika virus (ZIKV) is highly neurotropic after crossing the placenta, inducing teratogenic effects that result in delayed development and microcephaly in infants. The available evidence for vertical transmission of this infection is based on placental studies showing alterations in trophoblastic tissue. However, complete characterization of ZIKV-infected placenta and involved pathways has yet to be fully clarified. This case report of placental ZIKV infection describes morphologic and molecular changes in the placenta. Hyperplasia of placental Hofbauer cells in chorionic villi and numerous histiocyte-like cells in the decidua were observed. The decidua, fibroblasts, and chorion, as well as circulating cells in the intravascular compartment stained positive for ZIKV envelop protein. Deciduitis was present on the maternal surface of the placenta, with a prevalence of lymphocytes associated with vasculitis. A high level of uncommitted CD3 T lymphocytes were present, in addition to CD4 and CD8 cells. Elevated expression of the apoptosis inhibitor, Bcl-2, was observed in syncytiotrophoblasts. These parameters may promote the persistence of ZIKV in placental tissue and transmission to the fetus.
 ...
PMID:Histopathologic Changes in Placental Tissue Associated With Vertical Transmission of Zika Virus. 3078 99