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Study · In vitro (cells) · 2009

8 results

Rescue of functional F508del cystic fibrosis transmembrane conductance regulator by vasoactive intestinal peptide in the human nasal epithelial cell line JME/CF15.

Rafferty S, Alcolado N, Norez C, Chappe F, Pelzer S, Becq F, Chappe V

The Journal of pharmacology and experimental therapeutics7 Jul 2009Cited by 13 (Europe PMC)

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 study8

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

  1. 01LabIn vitro (cells)Activity measurement

    In human nasal epithelial JME/CF15 cells, one hour of VIP treatment strongly increased F508del-CFTR activity, with iodide efflux peaks three times higher than in untreated cells.

    In plain wordsIn cells with the cystic fibrosis mutation, VIP raised the activity of the faulty chloride channel about threefold compared with untreated cells.

    Outcome
    IncreaseF508del-CFTR activity after 1 h VIP
    Study

    humann: not reported in source

    JME/CF15 human nasal epithelial cell line (F508del-CFTR)
    Comparator
    Untreated cells
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated · 1 hourAs given in this study (human).

    Source sentences

    Summary
    One hour of treatment with VIP strongly increased F508del-CFTR activity, with iodide efflux peaks three times higher than with untreated cells.
    1 context sentence
    Summary · context
    In the present study, we investigated the effect of VIP on F508del-CFTR activity and membrane insertion in the human nasal epithelial cell line JME/CF15, which also expresses the VPAC(1) receptor.
  2. 02LabIn vitro (cells)Activity measurement

    In JME/CF15 cells at 37 degrees C, VIP-treated cells but not untreated controls showed significant iodide efflux peaks that were sensitive to the CFTR inhibitor CFTR(inh)-172.

    In plain wordsIn cells with the cystic fibrosis mutation at body temperature, VIP-treated cells showed channel activity that untreated cells did not.

    Outcome
    IncreaseCFTR-dependent iodide efflux at 37 C
    Study

    humann: not reported in source

    JME/CF15 human nasal epithelial cell line (F508del-CFTR)
    Comparator
    Untreated cells
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    At 37 degrees C, VIP-treated cells, but not untreated controls, showed significant iodide efflux peaks that were sensitive to the CFTR inhibitor
    1 context sentence
    Summary · context
    In the present study, we investigated the effect of VIP on F508del-CFTR activity and membrane insertion in the human nasal epithelial cell line JME/CF15, which also expresses the VPAC(1) receptor.
  3. 03LabIn vitro (cells)Mechanism

    In JME/CF15 cells at 37 degrees C, VIP induced maturation and membrane insertion of F508del-CFTR.

    In plain wordsIn cells with the cystic fibrosis mutation, VIP helped the faulty channel protein mature and reach the cell surface.

    Outcome
    IncreaseF508del-CFTR maturation and membrane insertion at 37 C
    Study

    humann: not reported in source

    JME/CF15 human nasal epithelial cell line (F508del-CFTR)
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Immunostaining, biotinylation assays, and Western blots confirmed a VIP-induced maturation and membrane insertion of F508del-CFTR at 37 degrees C.
    1 context sentence
    Summary · context
    In the present study, we investigated the effect of VIP on F508del-CFTR activity and membrane insertion in the human nasal epithelial cell line JME/CF15, which also expresses the VPAC(1) receptor.
  4. 04LabIn vitro (cells)Mechanism

    In JME/CF15 cells at reduced temperature (27 degrees C), acute VIP stimulation of rescued F508del-CFTR channels depended on protein kinase A and protein kinase C.

    In plain wordsIn cells, VIP's quick boost of the rescued channel needed two cell signaling enzymes, PKA and PKC.

    Outcome
    Not applicablePKA and PKC dependence of acute VIP stimulation at 27 C
    Study

    humann: not reported in source

    JME/CF15 human nasal epithelial cell line (F508del-CFTR)
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    At reduced temperature (27 degrees C), which rescues F508del-CFTR trafficking, acute stimulation by VIP of rescued F508del-CFTR channels was protein kinase A (PKA)- and PKC-dependent.
    1 context sentence
    Summary · context
    In the present study, we investigated the effect of VIP on F508del-CFTR activity and membrane insertion in the human nasal epithelial cell line JME/CF15, which also expresses the VPAC(1) receptor.
  5. 05LabIn vitro (cells)Mechanism

    In JME/CF15 cells, the PKA inhibitor H89 abolished the corrector effect of VIP on F508del-CFTR.

    In plain wordsIn cells, blocking the enzyme PKA removed VIP's ability to correct the faulty channel.

    Outcome
    DecreaseEffect of PKA inhibitor H89 on VIP corrector effect
    Study

    humann: not reported in source

    JME/CF15 human nasal epithelial cell line (F508del-CFTR)
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The corrector effect of VIP was abolished by the PKA inhibitor N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamidedihydrochloride (H89)
    1 context sentence
    Summary · context
    In the present study, we investigated the effect of VIP on F508del-CFTR activity and membrane insertion in the human nasal epithelial cell line JME/CF15, which also expresses the VPAC(1) receptor.
  6. 06LabIn vitro (cells)Mechanism

    In JME/CF15 cells, membrane localization but not maturation of F508del-CFTR was significantly reduced by the PKC inhibitor bisindolylmaleimide X and the Gi/o protein inhibitor pertussis toxin.

    In plain wordsIn cells, blocking PKC or Gi/o proteins reduced how much of the channel reached the cell surface.

    Outcome
    DecreaseEffect of PKC and Gi/o inhibitors on F508del-CFTR membrane localization
    Study

    humann: not reported in source

    JME/CF15 human nasal epithelial cell line (F508del-CFTR)
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    On the other hand, membrane localization, but not maturation, of F508del-CFTR was significantly reduced by the PKC inhibitor bisindolylmaleimide X and the G(i/o) protein inhibitor pertussis toxin.
    1 context sentence
    Summary · context
    In the present study, we investigated the effect of VIP on F508del-CFTR activity and membrane insertion in the human nasal epithelial cell line JME/CF15, which also expresses the VPAC(1) receptor.
  7. 07LabIn vitro (cells)Mechanism

    In JME/CF15 cells, VIP treatment had no effect on intracellular calcium.

    In plain wordsIn cells, VIP did not change calcium levels inside the cells.

    Outcome
    No significant changeIntracellular calcium after VIP
    Study

    humann: not reported in source

    JME/CF15 human nasal epithelial cell line (F508del-CFTR)
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    VIP treatment had no effect on intracellular calcium
    1 context sentence
    Summary · context
    In the present study, we investigated the effect of VIP on F508del-CFTR activity and membrane insertion in the human nasal epithelial cell line JME/CF15, which also expresses the VPAC(1) receptor.
  8. 08LabIn vitro (cells)Mechanism

    In JME/CF15 cells, VIP treatment had no effect on proteasome activity.

    In plain wordsIn cells, VIP did not change the activity of the cell's protein-disposal machinery.

    Outcome
    No significant changeProteasome activity after VIP
    Study

    humann: not reported in source

    JME/CF15 human nasal epithelial cell line (F508del-CFTR)
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    VIP treatment had no effect on intracellular calcium or proteasome activity
    1 context sentence
    Summary · context
    In the present study, we investigated the effect of VIP on F508del-CFTR activity and membrane insertion in the human nasal epithelial cell line JME/CF15, which also expresses the VPAC(1) receptor.

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

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