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Study · Animal study (in vivo) · mouse · 2015

11 results

Exendin-4 promotes endothelial barrier enhancement via PKA- and Epac1-dependent Rac1 activation.

Li AQ, Zhao L, Zhou TF, Zhang MQ, Qin XM

American journal of physiology. Cell physiology5 Nov 2014Cited by 28 (Europe PMC)

PMID25377089 (opens in a new tab)DOI10.1152/ajpcell.00249.2014 (opens in a new tab)PepBankPUB-25377089
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 study11

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice, exendin‑4 attenuated thrombin-induced subcutaneous vascular leakage.

    In plain wordsIn mice, exendin‑4 reduced blood vessel leakage caused by thrombin.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseVascular leakage
    Study

    mousen: not reported in source

    thrombin-induced subcutaneous vascular leakage
    Comparator
    thrombin challenge
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Here we show for the first time that the stable GLP-1 analog exendin-4 attenuated the leakage of subcutaneous blood vessels in mice indexed by dye extravasation caused by injections of thrombin.
  2. 02LabIn vitro (cells)Efficacy outcome

    In cultured endothelial cells, exendin‑4 prevented thrombin-induced FITC-dextran permeability via the GLP-1 receptor.

    In plain wordsIn cells, exendin‑4 reduced leakage caused by thrombin.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseEndothelial permeability
    Study

    n: not reported in source

    cultured endothelial cells
    Comparator
    thrombin challenge
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, in cultured endothelial cells, exendin-4 significantly prevented the thrombin-induced FITC-dextran permeability of endothelial monolayers via GLP-1 receptor.
  3. 03LabIn vitro (cells)Mechanism

    In endothelial cells, exendin‑4 prevented detrimental thrombin effects on VE-cadherin.

    In plain wordsIn cells, exendin‑4 prevented thrombin damage to VE-cadherin.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseVE-cadherin disruption
    Study

    n: not reported in source

    cultured endothelial cells
    Comparator
    thrombin challenge
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Immunofluorescence microscopy reveals that exendin-4 abrogates detrimental effects of thrombin on VE-cadherin and the F-actin cytoskeleton, with decreased stress fiber and gap formation.
  4. 04LabIn vitro (cells)Mechanism

    In endothelial cells, exendin‑4 decreased thrombin-induced stress fiber formation.

    In plain wordsIn cells, exendin‑4 reduced stress fibers caused by thrombin.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseStress fiber formation
    Study

    n: not reported in source

    cultured endothelial cells
    Comparator
    thrombin challenge
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Immunofluorescence microscopy reveals that exendin-4 abrogates detrimental effects of thrombin on VE-cadherin and the F-actin cytoskeleton, with decreased stress fiber and gap formation.
  5. 05LabIn vitro (cells)Mechanism

    In endothelial cells, exendin‑4 decreased thrombin-induced gap formation.

    In plain wordsIn cells, exendin‑4 reduced gaps caused by thrombin.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseGap formation
    Study

    n: not reported in source

    cultured endothelial cells
    Comparator
    thrombin challenge
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Immunofluorescence microscopy reveals that exendin-4 abrogates detrimental effects of thrombin on VE-cadherin and the F-actin cytoskeleton, with decreased stress fiber and gap formation.
  6. 06LabIn vitro (cells)Mechanism

    In endothelial cells, exendin‑4 reduced thrombin-induced VE-cadherin phosphorylation at Y731.

    In plain wordsIn cells, exendin‑4 reduced thrombin-induced VE-cadherin phosphorylation at Y731.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseVE-cadherin Y731 phosphorylation
    Study

    n: not reported in source

    cultured endothelial cells
    Comparator
    thrombin challenge
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Importantly, exendin-4 reduced thrombin-induced tyrosine phosphorylation of VE-cadherin at Y731 and Y658.
  7. 07LabIn vitro (cells)Mechanism

    In endothelial cells, exendin‑4 reduced thrombin-induced VE-cadherin phosphorylation at Y658.

    In plain wordsIn cells, exendin‑4 reduced thrombin-induced VE-cadherin phosphorylation at Y658.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseVE-cadherin Y658 phosphorylation
    Study

    n: not reported in source

    cultured endothelial cells
    Comparator
    thrombin challenge
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Importantly, exendin-4 reduced thrombin-induced tyrosine phosphorylation of VE-cadherin at Y731 and Y658.
  8. 08LabIn vitro (cells)Mechanism

    In endothelial cells, exendin‑4 significantly activated Rac1.

    In plain wordsIn cells, exendin‑4 activated Rac1.

    Peptide
    Exenatide (exendin-4)
    Outcome
    IncreaseRac1 activation
    Study

    n: not reported in source

    cultured endothelial cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, small GTPase Rac1 was significantly activated as a result of exendin-4 treatment.

Studies that did not test the peptide alone3

In this study, Exenatide (exendin-4) 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 Exenatide (exendin-4).

  1. 09LabNot a test of Exenatide (exendin-4) aloneIn vitro (cells)Mechanism

    In endothelial cells, Rac1 inhibition blunted exendin‑4 protection against thrombin-induced barrier disruption.

    In plain wordsIn cells, Rac1 inhibition weakened exendin‑4 barrier protection compared with exendin‑4 without inhibition.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseRac1-dependent barrier protection
    Study

    n: not reported in source

    cultured endothelial cells
    Comparator
    exendin-4 without Rac1 inhibition
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    The efficacy of exendin-4 to counteract the barrier-compromising effect of thrombin was blunted when Rac1 was inactivated by Rac1 inhibitor NSC-23766.

    In this study, Exenatide (exendin-4) 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 Exenatide (exendin-4).

  2. 10LabNot a test of Exenatide (exendin-4) aloneIn vitro (cells)Mechanism

    In endothelial cells, PKA inhibition or Epac1 silencing reduced exendin‑4-induced Rac1 activation.

    In plain wordsIn cells, PKA inhibition or Epac1 silencing reduced Rac1 activation compared with exendin‑4 alone.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreasePKA/Epac1-dependent Rac1 activation
    Study

    n: not reported in source

    cultured endothelial cells
    Comparator
    exendin-4 without PKA inhibition or Epac1 silencing
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Inhibition of PKA activity or small-interfering RNA for exchange protein directly activated by cAMP 1 (Epac1) decreased exendin-4-induced Rac1 activation and barrier enhancement, indicating the participation of both PKA and Epac1 in the barrier-stabilizing effect of exendin-4 elicited on thrombin-im…

    In this study, Exenatide (exendin-4) 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 Exenatide (exendin-4).

  3. 11LabNot a test of Exenatide (exendin-4) aloneIn vitro (cells)Mechanism

    In endothelial cells, PKA inhibition or Epac1 silencing reduced exendin‑4-induced barrier enhancement.

    In plain wordsIn cells, PKA inhibition or Epac1 silencing reduced barrier enhancement compared with exendin‑4 alone.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreasePKA/Epac1-dependent barrier enhancement
    Study

    n: not reported in source

    cultured endothelial cells
    Comparator
    exendin-4 without PKA inhibition or Epac1 silencing
    Outcome group
    Vascular function · Cardiovascular

    Source sentences

    Summary
    Inhibition of PKA activity or small-interfering RNA for exchange protein directly activated by cAMP 1 (Epac1) decreased exendin-4-induced Rac1 activation and barrier enhancement, indicating the participation of both PKA and Epac1 in the barrier-stabilizing effect of exendin-4 elicited on thrombin-im…

    In this study, Exenatide (exendin-4) 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 Exenatide (exendin-4).

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

    22 Oct 2026, 02:26 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 18:59 UTC

    First added · source update from Europe PMC

Subjects

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