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Study · In vitro (cells) · 2020

9 results

Protective Mechanism of the Selective Vasopressin V1A Receptor Agonist Selepressin against Endothelial Barrier Dysfunction.

Barabutis N, Marinova M, Solopov P, Uddin MA, Croston GE, Reinheimer TM, Catravas JD

The Journal of pharmacology and experimental therapeutics17 Sept 2020Cited by 12 (Europe PMC)

PMID32943478 (opens in a new tab)DOI10.1124/jpet.120.000146 (opens in a new tab)PepBankPUB-32943478
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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 study9

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

  1. 01LabIn vitro (cells)Mechanism

    In human lung endothelial cells, selepressin counteracted thrombin-induced barrier disruption in a concentration-dependent manner.

    In plain wordsIn cells, selepressin reduced thrombin-induced leakage across human lung blood vessel cell layers in a concentration-dependent manner.

    Peptide
    Selepressin
    Outcome
    DecreaseThrombin-induced hyperpermeability
    Study

    humann: not reported in source

    Cultured lung microvascular endothelial cells
    Outcome group
    Vascular function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Results suggest that selepressin counteracts the effects of all four endothelial barrier disruptors in a concentration-dependent manner, as reflected in real-time measurements of vascular permeability by means of transendothelial electrical resistance.
    1 context sentence
    Summary · context
    The effects of the selective V1AR-selective agonist selepressin have been investigated in an in vitro model of thrombin-, vascular endothelial growth factor-, angiopoietin 2-, and lipopolysaccharide (LPS)-induced pulmonary microvascular endothelial hyperpermeability.
  2. 02LabIn vitro (cells)Mechanism

    In human lung endothelial cells, selepressin counteracted vascular endothelial growth factor-induced barrier disruption in a concentration-dependent manner.

    In plain wordsIn cells, selepressin reduced vascular endothelial growth factor-induced leakage across human lung blood vessel cell layers.

    Peptide
    Selepressin
    Outcome
    DecreaseVEGF-induced hyperpermeability
    Study

    humann: not reported in source

    Cultured lung microvascular endothelial cells
    Outcome group
    Vascular function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Results suggest that selepressin counteracts the effects of all four endothelial barrier disruptors in a concentration-dependent manner, as reflected in real-time measurements of vascular permeability by means of transendothelial electrical resistance.
    1 context sentence
    Summary · context
    The effects of the selective V1AR-selective agonist selepressin have been investigated in an in vitro model of thrombin-, vascular endothelial growth factor-, angiopoietin 2-, and lipopolysaccharide (LPS)-induced pulmonary microvascular endothelial hyperpermeability.
  3. 03LabIn vitro (cells)Mechanism

    In human lung endothelial cells, selepressin counteracted angiopoietin 2-induced barrier disruption in a concentration-dependent manner.

    In plain wordsIn cells, selepressin reduced angiopoietin 2-induced leakage across human lung blood vessel cell layers in a concentration-dependent manner.

    Peptide
    Selepressin
    Outcome
    DecreaseAngiopoietin 2-induced hyperpermeability
    Study

    humann: not reported in source

    Cultured lung microvascular endothelial cells
    Outcome group
    Vascular function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Results suggest that selepressin counteracts the effects of all four endothelial barrier disruptors in a concentration-dependent manner, as reflected in real-time measurements of vascular permeability by means of transendothelial electrical resistance.
    1 context sentence
    Summary · context
    The effects of the selective V1AR-selective agonist selepressin have been investigated in an in vitro model of thrombin-, vascular endothelial growth factor-, angiopoietin 2-, and lipopolysaccharide (LPS)-induced pulmonary microvascular endothelial hyperpermeability.
  4. 04LabIn vitro (cells)Mechanism

    In human lung endothelial cells, selepressin counteracted LPS-induced barrier disruption in a concentration-dependent manner.

    In plain wordsIn cells, selepressin reduced LPS-induced leakage across human lung blood vessel cell layers in a concentration-dependent manner.

    Peptide
    Selepressin
    Outcome
    DecreaseLPS-induced hyperpermeability
    Study

    humann: not reported in source

    Cultured lung microvascular endothelial cells
    Outcome group
    Vascular function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Results suggest that selepressin counteracts the effects of all four endothelial barrier disruptors in a concentration-dependent manner, as reflected in real-time measurements of vascular permeability by means of transendothelial electrical resistance.
    1 context sentence
    Summary · context
    The effects of the selective V1AR-selective agonist selepressin have been investigated in an in vitro model of thrombin-, vascular endothelial growth factor-, angiopoietin 2-, and lipopolysaccharide (LPS)-induced pulmonary microvascular endothelial hyperpermeability.
  5. 05LabIn vitro (cells)Mechanism

    In human lung endothelial cells, selepressin protected LPS-challenged barrier integrity, assessed by VE-cadherin and actin staining.

    In plain wordsIn cells, selepressin protected human lung blood vessel cell layer integrity against LPS damage.

    Peptide
    Selepressin
    Outcome
    IncreaseEndothelial monolayer integrity
    Study

    humann: not reported in source

    Cultured lung microvascular endothelial cells
    Outcome group
    Vascular function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Further, selepressin protected the barrier integrity against the LPS-mediated corruption of the endothelial monolayer integrity, as captured by VE-cadherin and actin staining.
    1 context sentence
    Summary · context
    The effects of the selective V1AR-selective agonist selepressin have been investigated in an in vitro model of thrombin-, vascular endothelial growth factor-, angiopoietin 2-, and lipopolysaccharide (LPS)-induced pulmonary microvascular endothelial hyperpermeability.
  6. 06LabIn vitro (cells)Mechanism

    In human lung endothelial cells, selepressin strongly induced p53 expression.

    In plain wordsIn cells, selepressin strongly increased p53 expression in human lung blood vessel cells.

    Peptide
    Selepressin
    Outcome
    Increasep53 expression
    Study

    humann: not reported in source

    Cultured lung microvascular endothelial cells
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    p53 appears to be involved in mediating these palliative effects, since selepressin strongly induced its expression levels, suppressed the inflammatory RhoA/myosin light chain2 pathway, and triggered the barrier-protective effects of the GTPase Rac1.
    1 context sentence
    Summary · context
    The effects of the selective V1AR-selective agonist selepressin have been investigated in an in vitro model of thrombin-, vascular endothelial growth factor-, angiopoietin 2-, and lipopolysaccharide (LPS)-induced pulmonary microvascular endothelial hyperpermeability.
  7. 07LabIn vitro (cells)Mechanism

    In human lung endothelial cells, selepressin suppressed the inflammatory RhoA/myosin light chain2 pathway.

    In plain wordsIn cells, selepressin suppressed an inflammatory RhoA pathway in human lung blood vessel cells.

    Peptide
    Selepressin
    Outcome
    DecreaseRhoA/myosin light chain2 pathway
    Study

    humann: not reported in source

    Cultured lung microvascular endothelial cells
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    p53 appears to be involved in mediating these palliative effects, since selepressin strongly induced its expression levels, suppressed the inflammatory RhoA/myosin light chain2 pathway, and triggered the barrier-protective effects of the GTPase Rac1.
    1 context sentence
    Summary · context
    The effects of the selective V1AR-selective agonist selepressin have been investigated in an in vitro model of thrombin-, vascular endothelial growth factor-, angiopoietin 2-, and lipopolysaccharide (LPS)-induced pulmonary microvascular endothelial hyperpermeability.
  8. 08LabIn vitro (cells)Mechanism

    In human lung endothelial cells, selepressin triggered barrier-protective effects of Rac1.

    In plain wordsIn cells, selepressin triggered Rac1-mediated protection of human lung blood vessel cell layers.

    Peptide
    Selepressin
    Outcome
    IncreaseRac1 barrier protection
    Study

    humann: not reported in source

    Cultured lung microvascular endothelial cells
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    p53 appears to be involved in mediating these palliative effects, since selepressin strongly induced its expression levels, suppressed the inflammatory RhoA/myosin light chain2 pathway, and triggered the barrier-protective effects of the GTPase Rac1.
    1 context sentence
    Summary · context
    The effects of the selective V1AR-selective agonist selepressin have been investigated in an in vitro model of thrombin-, vascular endothelial growth factor-, angiopoietin 2-, and lipopolysaccharide (LPS)-induced pulmonary microvascular endothelial hyperpermeability.

Studies that did not test the peptide alone1

In this study, Selepressin 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 Selepressin.

  1. 09LabNot a test of Selepressin aloneIn vitro (cells)Mechanism

    In human lung endothelial cells, V1A receptor silencing abolished selepressin barrier protection.

    In plain wordsIn cells, silencing the V1A receptor abolished selepressin protection of human lung blood vessel cell layers.

    Peptide
    Selepressin
    Outcome
    Not applicableV1A receptor dependence
    Study

    humann: not reported in source

    Cultured lung microvascular endothelial cells
    Outcome group
    Vascular function · Respiratory

    Source sentences

    Summary
    The protective effects of selepressin were abolished by silencing of the vasopressin V1AR, as well as by atosiban, an antagonist of the human V1AR.
    1 context sentence
    Summary · context
    The effects of the selective V1AR-selective agonist selepressin have been investigated in an in vitro model of thrombin-, vascular endothelial growth factor-, angiopoietin 2-, and lipopolysaccharide (LPS)-induced pulmonary microvascular endothelial hyperpermeability.

    In this study, Selepressin 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 Selepressin.

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

    27 Oct 2026, 18:20 UTC

    Study results updated

  2. Version 1

    27 Oct 2026, 16:32 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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