A human pituitary tumor-derived folliculostellate cell line

被引:43
作者
Danila, DC
Zhang, X
Zhou, YL
Dickersin, GR
Fletcher, JA
Hedley-Whyte, ET
Selig, MK
Johnson, SR
Klibanski, A
机构
[1] Massachusetts Gen Hosp, Neuroendocrine Unit, Boston, MA 02115 USA
[2] Massachusetts Gen Hosp, Dept Pathol, Boston, MA 02115 USA
[3] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA
[4] Harvard Univ, Sch Med, Boston, MA 02115 USA
关键词
D O I
10.1210/jc.85.3.1180
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 5-100 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.
引用
收藏
页码:1180 / 1187
页数:8
相关论文
共 77 条
[1]   Tumor-specific expression and alternate splicing of messenger ribonucleic acid encoding activin transforming growth factor-beta receptors in human pituitary adenomas [J].
Alexander, JM ;
Bikkal, HA ;
Zervas, NT ;
Laws, ER ;
Klibanski, A .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1996, 81 (02) :783-790
[2]   HUMAN PITUITARY-ADENOMAS EXPRESS ENDOGENOUS INHIBIN SUBUNIT AND FOLLISTATIN MESSENGER RIBONUCLEIC-ACIDS [J].
ALEXANDER, JM ;
SWEARINGEN, B ;
TINDALL, GT ;
KLIBANSKI, A .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1995, 80 (01) :147-152
[3]   THE EFFECTS OF ACTIVIN ON FOLLICLE-STIMULATING-HORMONE SECRETION AND BIOSYNTHESIS IN HUMAN GLYCOPROTEIN HORMONE-PRODUCING PITUITARY-ADENOMAS [J].
ALEXANDER, JM ;
JAMESON, JL ;
BIKKAL, HA ;
SCHWALL, RH ;
KLIBANSKI, A .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1991, 72 (06) :1261-1267
[4]   The cytogenesis and pathogenesis of pituitary adenomas [J].
Asa, SL ;
Ezzat, S .
ENDOCRINE REVIEWS, 1998, 19 (06) :798-827
[5]   EVIDENCE THAT STIMULATION OF GROWTH-HORMONE RELEASE BY EPINEPHRINE AND VASOACTIVE-INTESTINAL-PEPTIDE IS BASED ON CELL-TO-CELL COMMUNICATION IN THE PITUITARY [J].
BAES, M ;
DENEF, C .
ENDOCRINOLOGY, 1987, 120 (01) :280-290
[6]   ISOLATION OF HUMAN-P53-SPECIFIC MONOCLONAL-ANTIBODIES AND THEIR USE IN THE STUDIES OF HUMAN P53 EXPRESSION [J].
BANKS, L ;
MATLASHEWSKI, G ;
CRAWFORD, L .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 1986, 159 (03) :529-534
[7]   INHIBITION OF SOMATOTROPH GROWTH AND GROWTH-HORMONE BIOSYNTHESIS BY ACTIVIN INVITRO [J].
BILLESTRUP, N ;
GONZALEZMANCHON, C ;
POTTER, E ;
VALE, W .
MOLECULAR ENDOCRINOLOGY, 1990, 4 (02) :356-362
[8]   INHIBIN, ACTIVIN, AND FOLLISTATIN - REGULATION OF FOLLICLE-STIMULATING-HORMONE MESSENGER-RIBONUCLEIC-ACID LEVELS [J].
CARROLL, RS ;
CORRIGAN, AZ ;
GHARIB, SD ;
VALE, W ;
CHIN, WW .
MOLECULAR ENDOCRINOLOGY, 1989, 3 (12) :1969-1976
[9]  
CASEY G, 1991, ONCOGENE, V6, P1791
[10]   A tumor-specific truncated estrogen receptor splice variant enhances estrogen-stimulated gene expression [J].
Chaidarun, SS ;
Alexander, JM .
MOLECULAR ENDOCRINOLOGY, 1998, 12 (09) :1355-1366