| A human pituitary tumor-derived folliculostellate cell line. | |
MedLine Citation:
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PMID: 10720059 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Pituitary cells have been used for the study of hormone synthesis, secretion, and regulation. However, the lack of human cell lines of pituitary origin has made such studies in humans very difficult. Activin, a member of the transforming growth factor-beta cytokine family, is secreted by the pituitary and serves, in addition to regulating hormone biosynthesis, as a regulator of cell growth and differentiation. In the human pituitary, folliculo-stellate cells secrete an activin-binding and -neutralizing protein, follistatin. However, the role of these cells in the autocrine/paracrine regulatory mechanisms of activin is poorly understood. We describe a human pituitary-derived folliculostellate cell line, designated PDFS, that was developed spontaneously from a clinically nonfunctioning pituitary macroadenoma. PDFS cells showed an epithelial-like morphology with long cytoplasmic processes. Electron microscopy revealed frequent intercellular junctions, including desmosomes, and cytogenetic analysis showed clonal characteristics with chromosomal abnormalities. These cells express vimentin and the nervous tissue-specific S-100 protein, specific markers of folliculostellate cells in the anterior pituitary, but no secretory pituitary cell markers. PDFS cells formed large colonies in an anchorage-independent transformation assay. They express follistatin and activin A and have an intact activin intracellular signaling pathway as determined by reporter assays. Therefore, this human cell line provides a useful model for studying the regulation of cell growth and cytokine production by factors endogenously produced in pituitary folliculostellate cells. |
Authors:
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D C Danila; X Zhang; Y Zhou; G R Dickersin; J A Fletcher; E T Hedley-Whyte; M K Selig; S R Johnson; A Klibanski |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: The Journal of clinical endocrinology and metabolism Volume: 85 ISSN: 0021-972X ISO Abbreviation: J. Clin. Endocrinol. Metab. Publication Date: 2000 Mar |
Date Detail:
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Created Date: 2000-03-30 Completed Date: 2000-03-30 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 0375362 Medline TA: J Clin Endocrinol Metab Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 1180-7 Citation Subset: AIM; IM |
Affiliation:
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Neuroendocrine Unit, Massachusetts General Hospital, Boston 02115, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Activin Receptors Activins Adenoma / genetics, pathology*, ultrastructure Aged Blotting, Western Cell Transformation, Neoplastic / pathology Chromosomes / ultrastructure Enzyme-Linked Immunosorbent Assay Follistatin Glycoproteins / biosynthesis, genetics Growth Substances / biosynthesis, genetics Humans Immunohistochemistry Inhibins / biosynthesis, genetics Luciferases / biosynthesis, genetics Male Microscopy, Electron Mutation / genetics Pituitary Neoplasms / genetics, pathology*, ultrastructure RNA, Messenger / biosynthesis Receptors, Growth Factor / biosynthesis, genetics Reverse Transcriptase Polymerase Chain Reaction Transfection / genetics Tumor Cells, Cultured Tumor Suppressor Protein p53 / genetics |
| Grant Support | |
ID/Acronym/Agency:
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P32-DK-07028/DK/NIDDK NIH HHS; R01-DK-40947/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Follistatin; 0/Glycoproteins; 0/Growth Substances; 0/RNA, Messenger; 0/Receptors, Growth Factor; 0/Tumor Suppressor Protein p53; 104625-48-1/Activins; 57285-09-3/Inhibins; EC 1.13.12.-/Luciferases; EC 2.7.11.30/Activin Receptors |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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