Stimulatory effect of insulin-like growth factor I on proliferation of mouse pituitary cells in serum-free culture

S. Oomizu, Sakae Takeuchi, S. Takahashi

Research output: Contribution to journalArticle

63 Citations (Scopus)

Abstract

IGF-I is synthesized in the human and rat anterior pituitary glands. The present study was designed to clarify the growth-promoting action of IGF-I on mouse pituitary cells in a primary serum-free culture system. Proliferation of pituitary cells was detected by monitoring the cellular uptake of bromodeoxyuridine (BrdU). BrdU labelling in the nucleus was found in all types of secretory cells: corticotrophs, thyrotrophs, gonadotrophs (LH cells and FSH cells), somatotrophs and mammotrophs. IGF-I (75 ng/ml) stimulated the proliferation of corticotrophs and mammotrophs among the pituitary secretory cells. IGF-I receptor mRNA was detected in the cultured pituitary cells using reverse transcription (RT)-PCR, indicating that mouse pituitary cells expressed IGF-I receptors. Insulin (100 ng/ml) or IGF-I (7.5 ng/ml) failed to increase the percentage of BrdU-labelled cells. However, treatment with insulin (100 ng/ml) plus IGF-I (7.5 ng/ml) increased the percentage of BrdU- labelled cells in a synergistic-like manner. Genistein, a tyrosine kinase specific inhibitor, decreased the IGF-I-induced cell proliferation, indicating that IGF-I acts through IGF-I receptors. IGF-I mRNA was also detected in the cultured pituitary cells by RT-PCR, and its peptides were immunocytochemically detected. The present results demonstrate that all types of pituitary secretory cells have the ability to proliferate in our serum- free culture system. IGF-I synthesized in the pituitary gland may stimulate the growth of pituitary cells, in particular corticotrophs and mammotrophs, by an autocrine or paracrine mechanism.

Original languageEnglish
Pages (from-to)53-62
Number of pages10
JournalJournal of Endocrinology
Volume157
Issue number1
DOIs
Publication statusPublished - Apr 1998

Fingerprint

Insulin-Like Growth Factor I
Serum
Corticotrophs
Bromodeoxyuridine
Gonadotrophs
IGF Type 1 Receptor
Reverse Transcription
Cultured Cells
Cell Proliferation
Thyrotrophs
Somatotrophs
Insulin
Polymerase Chain Reaction
Messenger RNA
Anterior Pituitary Gland
Genistein
Pituitary Gland
Growth
Protein-Tyrosine Kinases
Peptides

ASJC Scopus subject areas

  • Endocrinology

Cite this

Stimulatory effect of insulin-like growth factor I on proliferation of mouse pituitary cells in serum-free culture. / Oomizu, S.; Takeuchi, Sakae; Takahashi, S.

In: Journal of Endocrinology, Vol. 157, No. 1, 04.1998, p. 53-62.

Research output: Contribution to journalArticle

@article{74e92aa9b0b8482d9aa8b6b575a5c980,
title = "Stimulatory effect of insulin-like growth factor I on proliferation of mouse pituitary cells in serum-free culture",
abstract = "IGF-I is synthesized in the human and rat anterior pituitary glands. The present study was designed to clarify the growth-promoting action of IGF-I on mouse pituitary cells in a primary serum-free culture system. Proliferation of pituitary cells was detected by monitoring the cellular uptake of bromodeoxyuridine (BrdU). BrdU labelling in the nucleus was found in all types of secretory cells: corticotrophs, thyrotrophs, gonadotrophs (LH cells and FSH cells), somatotrophs and mammotrophs. IGF-I (75 ng/ml) stimulated the proliferation of corticotrophs and mammotrophs among the pituitary secretory cells. IGF-I receptor mRNA was detected in the cultured pituitary cells using reverse transcription (RT)-PCR, indicating that mouse pituitary cells expressed IGF-I receptors. Insulin (100 ng/ml) or IGF-I (7.5 ng/ml) failed to increase the percentage of BrdU-labelled cells. However, treatment with insulin (100 ng/ml) plus IGF-I (7.5 ng/ml) increased the percentage of BrdU- labelled cells in a synergistic-like manner. Genistein, a tyrosine kinase specific inhibitor, decreased the IGF-I-induced cell proliferation, indicating that IGF-I acts through IGF-I receptors. IGF-I mRNA was also detected in the cultured pituitary cells by RT-PCR, and its peptides were immunocytochemically detected. The present results demonstrate that all types of pituitary secretory cells have the ability to proliferate in our serum- free culture system. IGF-I synthesized in the pituitary gland may stimulate the growth of pituitary cells, in particular corticotrophs and mammotrophs, by an autocrine or paracrine mechanism.",
author = "S. Oomizu and Sakae Takeuchi and S. Takahashi",
year = "1998",
month = "4",
doi = "10.1677/joe.0.1570053",
language = "English",
volume = "157",
pages = "53--62",
journal = "Journal of Endocrinology",
issn = "0022-0795",
publisher = "Society for Endocrinology",
number = "1",

}

TY - JOUR

T1 - Stimulatory effect of insulin-like growth factor I on proliferation of mouse pituitary cells in serum-free culture

AU - Oomizu, S.

AU - Takeuchi, Sakae

AU - Takahashi, S.

PY - 1998/4

Y1 - 1998/4

N2 - IGF-I is synthesized in the human and rat anterior pituitary glands. The present study was designed to clarify the growth-promoting action of IGF-I on mouse pituitary cells in a primary serum-free culture system. Proliferation of pituitary cells was detected by monitoring the cellular uptake of bromodeoxyuridine (BrdU). BrdU labelling in the nucleus was found in all types of secretory cells: corticotrophs, thyrotrophs, gonadotrophs (LH cells and FSH cells), somatotrophs and mammotrophs. IGF-I (75 ng/ml) stimulated the proliferation of corticotrophs and mammotrophs among the pituitary secretory cells. IGF-I receptor mRNA was detected in the cultured pituitary cells using reverse transcription (RT)-PCR, indicating that mouse pituitary cells expressed IGF-I receptors. Insulin (100 ng/ml) or IGF-I (7.5 ng/ml) failed to increase the percentage of BrdU-labelled cells. However, treatment with insulin (100 ng/ml) plus IGF-I (7.5 ng/ml) increased the percentage of BrdU- labelled cells in a synergistic-like manner. Genistein, a tyrosine kinase specific inhibitor, decreased the IGF-I-induced cell proliferation, indicating that IGF-I acts through IGF-I receptors. IGF-I mRNA was also detected in the cultured pituitary cells by RT-PCR, and its peptides were immunocytochemically detected. The present results demonstrate that all types of pituitary secretory cells have the ability to proliferate in our serum- free culture system. IGF-I synthesized in the pituitary gland may stimulate the growth of pituitary cells, in particular corticotrophs and mammotrophs, by an autocrine or paracrine mechanism.

AB - IGF-I is synthesized in the human and rat anterior pituitary glands. The present study was designed to clarify the growth-promoting action of IGF-I on mouse pituitary cells in a primary serum-free culture system. Proliferation of pituitary cells was detected by monitoring the cellular uptake of bromodeoxyuridine (BrdU). BrdU labelling in the nucleus was found in all types of secretory cells: corticotrophs, thyrotrophs, gonadotrophs (LH cells and FSH cells), somatotrophs and mammotrophs. IGF-I (75 ng/ml) stimulated the proliferation of corticotrophs and mammotrophs among the pituitary secretory cells. IGF-I receptor mRNA was detected in the cultured pituitary cells using reverse transcription (RT)-PCR, indicating that mouse pituitary cells expressed IGF-I receptors. Insulin (100 ng/ml) or IGF-I (7.5 ng/ml) failed to increase the percentage of BrdU-labelled cells. However, treatment with insulin (100 ng/ml) plus IGF-I (7.5 ng/ml) increased the percentage of BrdU- labelled cells in a synergistic-like manner. Genistein, a tyrosine kinase specific inhibitor, decreased the IGF-I-induced cell proliferation, indicating that IGF-I acts through IGF-I receptors. IGF-I mRNA was also detected in the cultured pituitary cells by RT-PCR, and its peptides were immunocytochemically detected. The present results demonstrate that all types of pituitary secretory cells have the ability to proliferate in our serum- free culture system. IGF-I synthesized in the pituitary gland may stimulate the growth of pituitary cells, in particular corticotrophs and mammotrophs, by an autocrine or paracrine mechanism.

UR - http://www.scopus.com/inward/record.url?scp=0031955451&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031955451&partnerID=8YFLogxK

U2 - 10.1677/joe.0.1570053

DO - 10.1677/joe.0.1570053

M3 - Article

VL - 157

SP - 53

EP - 62

JO - Journal of Endocrinology

JF - Journal of Endocrinology

SN - 0022-0795

IS - 1

ER -