Effects of protein kinase A inhibitor (H-89) on VIP- and GRF-induced release and mRNA expression of prolactin and growth hormone in the chicken pituitary gland

Norio Kansaku, Kiyoshi Shimada, Noboru Saito, Hiroyoshi Hidaka

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Vasoactive intestinal polypeptide (VIP) and growth hormone releasing factor (GRF) stimulated an increase of cAMP accumulation with a concomitant release of PRL and GH, respectively. Release of PRL induced by VIP was partially suppressed by 5 and 25 μM of H-89, whereas VIP-induced gene expression of PRL was inhibited by all concentrations of H-89. Release and gene expression of GH induced by GRF was inhibited by H-89 in a dose dependent manner and completely blocked by 25 μM of H-89. These results indicate that VIP-induced PRL release and gene expression may be mediated, at least in a part, by cAMP-dependent protein kinase pachway, whereas GRF-induced GH release and gene expression may be mediated predominantly by cAMP dependent protein kinase.

Original languageEnglish
Pages (from-to)89-95
Number of pages7
JournalComparative Biochemistry and Physiology - C Pharmacology Toxicology and Endocrinology
Volume119
Issue number1
DOIs
Publication statusPublished - Jan 1998
Externally publishedYes

Fingerprint

Gastrointestinal Hormones
Growth Hormone-Releasing Hormone
Peptide Hormones
Vasoactive Intestinal Peptide
Pituitary Gland
Protein Kinase Inhibitors
Cyclic AMP-Dependent Protein Kinases
Prolactin
Growth Hormone
Chickens
Gene Expression
Messenger RNA
N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide

Keywords

  • cAMP
  • Forskolin
  • GH
  • GRF
  • H-89
  • mRMNA expression
  • PKA
  • PRL
  • VIP

ASJC Scopus subject areas

  • Pharmacology
  • Immunology

Cite this

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title = "Effects of protein kinase A inhibitor (H-89) on VIP- and GRF-induced release and mRNA expression of prolactin and growth hormone in the chicken pituitary gland",
abstract = "Vasoactive intestinal polypeptide (VIP) and growth hormone releasing factor (GRF) stimulated an increase of cAMP accumulation with a concomitant release of PRL and GH, respectively. Release of PRL induced by VIP was partially suppressed by 5 and 25 μM of H-89, whereas VIP-induced gene expression of PRL was inhibited by all concentrations of H-89. Release and gene expression of GH induced by GRF was inhibited by H-89 in a dose dependent manner and completely blocked by 25 μM of H-89. These results indicate that VIP-induced PRL release and gene expression may be mediated, at least in a part, by cAMP-dependent protein kinase pachway, whereas GRF-induced GH release and gene expression may be mediated predominantly by cAMP dependent protein kinase.",
keywords = "cAMP, Forskolin, GH, GRF, H-89, mRMNA expression, PKA, PRL, VIP",
author = "Norio Kansaku and Kiyoshi Shimada and Noboru Saito and Hiroyoshi Hidaka",
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T1 - Effects of protein kinase A inhibitor (H-89) on VIP- and GRF-induced release and mRNA expression of prolactin and growth hormone in the chicken pituitary gland

AU - Kansaku, Norio

AU - Shimada, Kiyoshi

AU - Saito, Noboru

AU - Hidaka, Hiroyoshi

PY - 1998/1

Y1 - 1998/1

N2 - Vasoactive intestinal polypeptide (VIP) and growth hormone releasing factor (GRF) stimulated an increase of cAMP accumulation with a concomitant release of PRL and GH, respectively. Release of PRL induced by VIP was partially suppressed by 5 and 25 μM of H-89, whereas VIP-induced gene expression of PRL was inhibited by all concentrations of H-89. Release and gene expression of GH induced by GRF was inhibited by H-89 in a dose dependent manner and completely blocked by 25 μM of H-89. These results indicate that VIP-induced PRL release and gene expression may be mediated, at least in a part, by cAMP-dependent protein kinase pachway, whereas GRF-induced GH release and gene expression may be mediated predominantly by cAMP dependent protein kinase.

AB - Vasoactive intestinal polypeptide (VIP) and growth hormone releasing factor (GRF) stimulated an increase of cAMP accumulation with a concomitant release of PRL and GH, respectively. Release of PRL induced by VIP was partially suppressed by 5 and 25 μM of H-89, whereas VIP-induced gene expression of PRL was inhibited by all concentrations of H-89. Release and gene expression of GH induced by GRF was inhibited by H-89 in a dose dependent manner and completely blocked by 25 μM of H-89. These results indicate that VIP-induced PRL release and gene expression may be mediated, at least in a part, by cAMP-dependent protein kinase pachway, whereas GRF-induced GH release and gene expression may be mediated predominantly by cAMP dependent protein kinase.

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