Paracrine stimulation of cell growth by cholecystokinin/gastrin through cholecystokinin-B receptor on GH3 cells in vitro

Yue Xu, Hidesuke Kaji, Yasuhiko Okimura, Toshimitu Matsui, Hiromi Abe, Kazuo Chihara

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

Cholecystokinin (CCK) is detected in pituitary tumors but its role remains unknown. On the hypothesis that CCK may facilitate the cell growth in pituitary tumors, we have examined the effect of CCK on cell growth using a rat pituitary tumor cell line, GH3, cultured in a serum-free, chemically defined medium. Addition of sulfated CCK-(26-33) (CCK-8) in twodifferent concentrations (0.5 ˜ 1 nM) causeda significant increase in the number of GH3 cells.The antagonist (1 μM) for CCK-B receptor, but not CCK-A receptor, significantly inhibited the number of GH3 cells. Northern blot analysis revealed asignificant expression of CCK-B receptor mRNA in GH3 cells, but notin normal rat pituitary glands. In addition, immunoreactive CCK/gastrin was detected by RIA in the GH3 cell extracts as well as the serum-free culture medium. In GH3 cell extracts, both CCK-8 and gastrin like peptides wereidentified by gel chromatography. These findings provided thefirst evidence for an autocrine/paracrine role of CCK and gastrinon stimulation of GH3 cell growth through the CCK-B receptor.

Original languageEnglish
Pages (from-to)280-285
Number of pages6
JournalNeuroendocrinology
Volume64
Issue number4
DOIs
StatePublished - 1996
Externally publishedYes

Keywords

  • Cholecystokinin
  • Cholecystokinin antagonists
  • Cholecystokinin receptors
  • GH cells
  • Gastrin

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