Document Detail


A human pituitary tumor-derived folliculostellate cell line.
MedLine Citation:
PMID:  10720059     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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:
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:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
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:
Created Date:  2000-03-30     Completed Date:  2000-03-30     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0375362     Medline TA:  J Clin Endocrinol Metab     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1180-7     Citation Subset:  AIM; IM    
Affiliation:
Neuroendocrine Unit, Massachusetts General Hospital, Boston 02115, USA.
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MeSH Terms
Descriptor/Qualifier:
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:
P32-DK-07028/DK/NIDDK NIH HHS; R01-DK-40947/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
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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