Estradiol and triiodothyronine increase production of insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding protein-3 (IGFBP-3) by GH4C1 rat pituitary tumor cells

Cindy A. Gilchrist, Jung H Y Park, Richard G MacDonald, James D. Shull

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

The main purpose of this study was to examine the effect of 17β-estradiol (E2) on the production of insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding proteins (IGFBP) by GH4C1 cells, a pituitary tumor cell line that displays many phenotypic properties of the anterior pituitary lactotroph. At a low population density (10 500 cells/cm2), E2 stimulated production of IGF-I by 4.2-fold. At this density, the antiestrogen tamoxifen (TAM) had no significant effect, whereas triiodothyronine (T3), which has been demonstrated to increase the level of IGF-I mRNA in the parental GH3 cell line, stimulated IGF-I production by 3.3-fold. Both E2 and T3 also stimulated GH4C1 cell proliferation at this population density. At a four-fold higher population density (42 000 cells/cm2), E2, TAM and T3 had little effect on IGF-I production. E2 failed to stimulate proliferation of GH4C1 cells at high density, and T3 stimulated production of IGFBP-3 by 6- and 11-fold, respectively. At high density, the abilities of E2 and T3 to stimulate IGFBP-3 production were somewhat reduced. TAM had no effect on IGFBP-3 production at either population density. These data indicate that E2 and T3 stimulate production by GH4C1 cells of IGF-I through a mechanism that is sensitive to changes in population density.

Original languageEnglish (US)
Pages (from-to)147-156
Number of pages10
JournalMolecular and Cellular Endocrinology
Volume114
Issue number1-2
DOIs
StatePublished - Oct 30 1995

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Insulin-Like Growth Factor Binding Protein 3
Pituitary Neoplasms
Triiodothyronine
Insulin-Like Growth Factor I
Rats
Tumors
Population Density
Estradiol
Cells
Tamoxifen
Insulin-Like Growth Factor Binding Protein 6
Cell Proliferation
Lactotrophs
Insulin-Like Growth Factor Binding Proteins
Estrogen Receptor Modulators
Tumor Cell Line
Cell proliferation
Cell Line
Messenger RNA

Keywords

  • Estradiol
  • Insulin-like growth factor binding protein
  • Insulin-like growth factor-I
  • Triiodothyronine

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Endocrinology

Cite this

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title = "Estradiol and triiodothyronine increase production of insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding protein-3 (IGFBP-3) by GH4C1 rat pituitary tumor cells",
abstract = "The main purpose of this study was to examine the effect of 17β-estradiol (E2) on the production of insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding proteins (IGFBP) by GH4C1 cells, a pituitary tumor cell line that displays many phenotypic properties of the anterior pituitary lactotroph. At a low population density (10 500 cells/cm2), E2 stimulated production of IGF-I by 4.2-fold. At this density, the antiestrogen tamoxifen (TAM) had no significant effect, whereas triiodothyronine (T3), which has been demonstrated to increase the level of IGF-I mRNA in the parental GH3 cell line, stimulated IGF-I production by 3.3-fold. Both E2 and T3 also stimulated GH4C1 cell proliferation at this population density. At a four-fold higher population density (42 000 cells/cm2), E2, TAM and T3 had little effect on IGF-I production. E2 failed to stimulate proliferation of GH4C1 cells at high density, and T3 stimulated production of IGFBP-3 by 6- and 11-fold, respectively. At high density, the abilities of E2 and T3 to stimulate IGFBP-3 production were somewhat reduced. TAM had no effect on IGFBP-3 production at either population density. These data indicate that E2 and T3 stimulate production by GH4C1 cells of IGF-I through a mechanism that is sensitive to changes in population density.",
keywords = "Estradiol, Insulin-like growth factor binding protein, Insulin-like growth factor-I, Triiodothyronine",
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T1 - Estradiol and triiodothyronine increase production of insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding protein-3 (IGFBP-3) by GH4C1 rat pituitary tumor cells

AU - Gilchrist, Cindy A.

AU - Park, Jung H Y

AU - MacDonald, Richard G

AU - Shull, James D.

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N2 - The main purpose of this study was to examine the effect of 17β-estradiol (E2) on the production of insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding proteins (IGFBP) by GH4C1 cells, a pituitary tumor cell line that displays many phenotypic properties of the anterior pituitary lactotroph. At a low population density (10 500 cells/cm2), E2 stimulated production of IGF-I by 4.2-fold. At this density, the antiestrogen tamoxifen (TAM) had no significant effect, whereas triiodothyronine (T3), which has been demonstrated to increase the level of IGF-I mRNA in the parental GH3 cell line, stimulated IGF-I production by 3.3-fold. Both E2 and T3 also stimulated GH4C1 cell proliferation at this population density. At a four-fold higher population density (42 000 cells/cm2), E2, TAM and T3 had little effect on IGF-I production. E2 failed to stimulate proliferation of GH4C1 cells at high density, and T3 stimulated production of IGFBP-3 by 6- and 11-fold, respectively. At high density, the abilities of E2 and T3 to stimulate IGFBP-3 production were somewhat reduced. TAM had no effect on IGFBP-3 production at either population density. These data indicate that E2 and T3 stimulate production by GH4C1 cells of IGF-I through a mechanism that is sensitive to changes in population density.

AB - The main purpose of this study was to examine the effect of 17β-estradiol (E2) on the production of insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding proteins (IGFBP) by GH4C1 cells, a pituitary tumor cell line that displays many phenotypic properties of the anterior pituitary lactotroph. At a low population density (10 500 cells/cm2), E2 stimulated production of IGF-I by 4.2-fold. At this density, the antiestrogen tamoxifen (TAM) had no significant effect, whereas triiodothyronine (T3), which has been demonstrated to increase the level of IGF-I mRNA in the parental GH3 cell line, stimulated IGF-I production by 3.3-fold. Both E2 and T3 also stimulated GH4C1 cell proliferation at this population density. At a four-fold higher population density (42 000 cells/cm2), E2, TAM and T3 had little effect on IGF-I production. E2 failed to stimulate proliferation of GH4C1 cells at high density, and T3 stimulated production of IGFBP-3 by 6- and 11-fold, respectively. At high density, the abilities of E2 and T3 to stimulate IGFBP-3 production were somewhat reduced. TAM had no effect on IGFBP-3 production at either population density. These data indicate that E2 and T3 stimulate production by GH4C1 cells of IGF-I through a mechanism that is sensitive to changes in population density.

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