Effects of vasoactive intestinal peptide on steroid secretion and plasminogen activator activity in granulosa cells of the hen.

Alan Leslie Johnson, J. L. Tilly

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Studies were conducted to evaluate the effects of vasoactive intestinal peptide (VIP) on steroidogenesis and plasminogen-activator (PA) activity in isolated granulosa cells of the largest preovulatory (F1) follicle of the hen. Vasoactive intestinal peptide, but not avian pancreatic polypeptide, the chicken VIP fragment (16-28) or the VIP congener, PHM-27, induced a dose-related increase in progesterone and androgen secretion, with an apparent median effective dose (ED50) of 5.9 X 10(-7) and 5.7 X 10(-7) M, respectively. The effects of VIP were, at least in part, mediated by the adenylyl cyclase system in that cotreatment of cells with VIP and the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (IBMX), potentiated the steroidogenic effects. However, the time course of action for VIP on steroidogenesis was considerably slower than that for the gonadotropin, luteinizing hormone (LH), and this was attributed to a slower induction of cyclic adenosine 3',5'-monophosphate (cAMP) formation within granulosa cells. Finally, VIP was found to be a potent inhibitor of PA activity, and this inhibition was potentiated by coincubation of VIP with IBMX. We suggest that, in the hen, VIP has a direct and specific action on both steroidogenesis and PA activity, and that these actions are mediated, at least in part, by the adenylyl cyclase system. The comparatively slow induction of cAMP formation by VIP suggests that this peptide is involved in the control of cell differentiation and development rather than the ovulatory process.

Original languageEnglish (US)
Pages (from-to)296-303
Number of pages8
JournalBiology of Reproduction
Volume38
Issue number2
DOIs
StatePublished - Jan 1 1988

Fingerprint

Granulosa Cells
Plasminogen Activators
Vasoactive Intestinal Peptide
Steroids
Peptide PHI
Adenylyl Cyclases
Cyclic AMP
Plasminogen Inactivators
1-Methyl-3-isobutylxanthine
Peptide Fragments
Phosphodiesterase Inhibitors
Luteinizing Hormone
Gonadotropins
Androgens
Progesterone
Cell Differentiation
Chickens

All Science Journal Classification (ASJC) codes

  • Reproductive Medicine
  • Cell Biology

Cite this

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abstract = "Studies were conducted to evaluate the effects of vasoactive intestinal peptide (VIP) on steroidogenesis and plasminogen-activator (PA) activity in isolated granulosa cells of the largest preovulatory (F1) follicle of the hen. Vasoactive intestinal peptide, but not avian pancreatic polypeptide, the chicken VIP fragment (16-28) or the VIP congener, PHM-27, induced a dose-related increase in progesterone and androgen secretion, with an apparent median effective dose (ED50) of 5.9 X 10(-7) and 5.7 X 10(-7) M, respectively. The effects of VIP were, at least in part, mediated by the adenylyl cyclase system in that cotreatment of cells with VIP and the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (IBMX), potentiated the steroidogenic effects. However, the time course of action for VIP on steroidogenesis was considerably slower than that for the gonadotropin, luteinizing hormone (LH), and this was attributed to a slower induction of cyclic adenosine 3',5'-monophosphate (cAMP) formation within granulosa cells. Finally, VIP was found to be a potent inhibitor of PA activity, and this inhibition was potentiated by coincubation of VIP with IBMX. We suggest that, in the hen, VIP has a direct and specific action on both steroidogenesis and PA activity, and that these actions are mediated, at least in part, by the adenylyl cyclase system. The comparatively slow induction of cAMP formation by VIP suggests that this peptide is involved in the control of cell differentiation and development rather than the ovulatory process.",
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Effects of vasoactive intestinal peptide on steroid secretion and plasminogen activator activity in granulosa cells of the hen. / Johnson, Alan Leslie; Tilly, J. L.

In: Biology of Reproduction, Vol. 38, No. 2, 01.01.1988, p. 296-303.

Research output: Contribution to journalArticle

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