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Study · In vitro (cells) · rat · 2000

6 results

Vasoactive intestinal polypeptide and pituitary adenylate cyclase-activating polypeptides stimulate mitogen-activated protein kinase in the pituitary cell line GH4C1 by a 3',5'-cyclic adenosine monophosphate pathway.

Le Péchon-Vallée C, Magalon K, Rasolonjanahary R, Enjalbert A, Gérard C

Neuroendocrinology1 Jul 2000Cited by 32 (Europe PMC)

PMID10940738 (opens in a new tab)DOI10.1159/000054570 (opens in a new tab)PepBankPUB-10940738
Publisher pagePubMedAsk about this study
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study6

5 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Mechanism

    In GH4C1 pituitary cells, VIP increased ERK1 and ERK2 phosphorylation, with potency equal to PACAP38.

    In plain wordsIn pituitary cells in the lab, VIP switched on the ERK signalling proteins, as strongly as PACAP38.

    Peptide
    Vasoactive intestinal peptide (VIP, aviptadil)
    Outcome
    IncreaseERK1 and ERK2 phosphorylation
    Study

    ratn: not reported in source

    GH4C1 somatolactotrope cell line
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    VIP and PACAP38 increased ERK1 and ERK2 phosphorylation and were equipotent stimulators of both kinases.
    1 context sentence
    Summary · context
    In this study, the control of the extracellularly responsive kinases (ERKs) by VIP and PACAP38 was investigated in GH4C1 cells.
  2. 02LabIn vitro (cells)Mechanism

    In GH4C1 cells, the protein kinase A inhibitor H89 blocked VIP activation of ERK2.

    In plain wordsIn pituitary cells in the lab, blocking protein kinase A stopped VIP from switching on ERK2.

    Peptide
    Vasoactive intestinal peptide (VIP, aviptadil)
    Outcome
    DecreaseProtein kinase A inhibition of VIP-induced ERK2 activation
    Study

    ratn: not reported in source

    GH4C1 somatolactotrope cell line
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    VIP and PACAP38 activation of ERK2 was blocked by the protein kinase A inhibitor H89
    1 context sentence
    Summary · context
    In this study, the control of the extracellularly responsive kinases (ERKs) by VIP and PACAP38 was investigated in GH4C1 cells.
  3. 03LabIn vitro (cells)Mechanism

    In GH4C1 cells, a protein kinase C inhibitor or depletion of protein kinases C did not inhibit VIP activation of ERK2.

    In plain wordsIn pituitary cells in the lab, blocking protein kinase C did not stop VIP from switching on ERK2.

    Peptide
    Vasoactive intestinal peptide (VIP, aviptadil)
    Outcome
    No significant changeProtein kinase C inhibition of VIP-induced ERK2 activation
    Study

    ratn: not reported in source

    GH4C1 somatolactotrope cell line
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    whereas the protein kinase C inhibitor GF109203X, or prior PMA-induced depletion of the protein kinases C, failed to inhibit VIP and PACAP38 activation of ERK2.
    1 context sentence
    Summary · context
    In this study, the control of the extracellularly responsive kinases (ERKs) by VIP and PACAP38 was investigated in GH4C1 cells.
  4. 04LabIn vitro (cells)Mechanism

    In GH4C1 cells, ERK activation by VIP or PACAP38 was sensitive to the MEK inhibitors PD98059 and U0126.

    In plain wordsIn pituitary cells in the lab, MEK-blocking drugs reduced the ERK activation caused by VIP.

    Peptide
    Vasoactive intestinal peptide (VIP, aviptadil)
    Outcome
    DecreaseMEK inhibitor sensitivity of VIP-induced ERK activation
    Study

    ratn: not reported in source

    GH4C1 somatolactotrope cell line
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and both sensitive to the MEK inhibitors PD98059 and U0126.
    1 context sentence
    Summary · context
    In this study, the control of the extracellularly responsive kinases (ERKs) by VIP and PACAP38 was investigated in GH4C1 cells.
  5. 05LabIn vitro (cells)Mechanism

    In GH4C1 cells, the MEK inhibitor U0126 reduced prolactin mRNA levels induced by VIP.

    In plain wordsIn pituitary cells in the lab, the MEK blocker U0126 lowered prolactin mRNA that VIP had raised.

    Peptide
    Vasoactive intestinal peptide (VIP, aviptadil)
    Outcome
    DecreaseProlactin mRNA induced by VIP
    Study

    ratn: not reported in source

    GH4C1 somatolactotrope cell line
    Outcome group
    Pituitary hormones · Endocrine and hormones
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In parallel, U0126 reduced prolactin (PRL) mRNA levels induced by VIP.
    1 context sentence
    Summary · context
    In this study, the control of the extracellularly responsive kinases (ERKs) by VIP and PACAP38 was investigated in GH4C1 cells.

Studies that did not test the peptide alone1

In this study, Vasoactive intestinal peptide (VIP, aviptadil) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Vasoactive intestinal peptide (VIP, aviptadil).

  1. 06LabNot a test of Vasoactive intestinal peptide (VIP, aviptadil) aloneIn vitro (cells)Mechanism

    In GH4C1 cells, ERK activation by VIP or PACAP38 and by TRH were additive.

    In plain wordsIn pituitary cells in the lab, VIP and TRH together switched on ERK more than either alone.

    Peptide
    Vasoactive intestinal peptide (VIP, aviptadil)
    Outcome
    Not applicableERK activation by VIP together with TRH
    Study

    ratn: not reported in source

    GH4C1 somatolactotrope cell line
    Outcome group
    Receptor activity and mechanism · Endocrine and hormones

    Source sentences

    Summary
    ERK activation by VIP or PACAP38 and TRH were additive
    1 context sentence
    Summary · context
    In this study, the control of the extracellularly responsive kinases (ERKs) by VIP and PACAP38 was investigated in GH4C1 cells.

    In this study, Vasoactive intestinal peptide (VIP, aviptadil) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Vasoactive intestinal peptide (VIP, aviptadil).

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    12 Oct 2026, 12:58 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 12:41 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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