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Study · In vitro (cells) · 2006

4 results

Binding of PAI-1 to endothelial cells stimulated by thymosin beta4 and modulation of their fibrinolytic potential.

Boncela J, Smolarczyk K, Wyroba E, Cierniewski CS

The Journal of biological chemistry4 Nov 2005Cited by 12 (Europe PMC)

PMID16272158 (opens in a new tab)DOI10.1074/jbc.m506303200 (opens in a new tab)PepBankPUB-16272158
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Summary

Our previous studies showed that thymosin beta4 (Tbeta4) induced the synthesis of plasminogen activator inhibitor-1 (PAI-1) in cultured human umbilical vein endothelial cells (HUVECs) via the AP-1 dependent mechanism and its enhanced secretion. In this work we provide evidence that the released PAI-1 is accumulated on the surface of HUVECs, exclusively in its active form, in a complex with alpha1-acid glycoprotein (AGP) that is also up-regulated and released from the cells. This mechanism is supported by several lines of experiments, in which expression of both proteins was analyzed by flow cytometry and their colocalization supported by confocal microscopy. PAI-1 did not bind to quiescent cells but only to the Tbeta4-activated endothelial cells. In contrast, significant amounts of AGP were found to be associated with the cells overexpressing enhanced green fluorescent protein (EGFP)-alpha1-acid glycoprotein (AGP) without Tbeta4 treatment. The AGP.PAI-1 complex was accumulated essentially at the basal surface of endothelial cells, and such cells showed (a) morphology characteristic for strongly adhered and spread cells and (b) significantly reduced plasmin formation. Taken together, these results provide the evidence supporting a novel mechanism by which active PAI-1 can be bound to the Tbeta4-activated endothelial cells, thus influencing their adhesive properties as well as their ability to generate plasmin.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study4

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

  1. 01LabIn vitro (cells)Mechanism

    In HUVECs, PAI-1 bound to Tbeta4-activated cells but not to quiescent cells.

    In plain wordsIn cells, PAI-1 attached to Tbeta4-treated endothelial cells but not to untreated resting cells.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreasePAI-1 binding to Tbeta4-activated versus quiescent endothelial cells
    Study

    humann: not reported in source

    cultured human umbilical vein endothelial cells (HUVECs)
    Comparator
    Quiescent cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    PAI-1 did not bind to quiescent cells but only to the Tbeta4-activated endothelial cells.
    1 context sentence
    Summary · context
    Our previous studies showed that thymosin beta4 (Tbeta4) induced the synthesis of plasminogen activator inhibitor-1 (PAI-1) in cultured human umbilical vein endothelial cells (HUVECs) via the AP-1 dependent mechanism and its enhanced secretion.
  2. 02LabIn vitro (cells)Mechanism

    In HUVECs treated with Tbeta4, released PAI-1 accumulated on the cell surface in active form, in a complex with up-regulated alpha1-acid glycoprotein.

    In plain wordsIn cells, Tbeta4 treatment led to PAI-1 collecting on the cell surface with alpha1-acid glycoprotein.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseAGP up-regulation and release with PAI-1 complex on cell surface
    Study

    humann: not reported in source

    cultured human umbilical vein endothelial cells (HUVECs)
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In this work we provide evidence that the released PAI-1 is accumulated on the surface of HUVECs, exclusively in its active form, in a complex with alpha1-acid glycoprotein (AGP) that is also up-regulated and released from the cells.
    1 context sentence
    Summary · context
    Our previous studies showed that thymosin beta4 (Tbeta4) induced the synthesis of plasminogen activator inhibitor-1 (PAI-1) in cultured human umbilical vein endothelial cells (HUVECs) via the AP-1 dependent mechanism and its enhanced secretion.
  3. 03LabIn vitro (cells)Mechanism

    In HUVECs, cells carrying the AGP.PAI-1 complex showed significantly reduced plasmin formation.

    In plain wordsIn cells, those with the AGP.PAI-1 complex made much less plasmin.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreasePlasmin formation by cells carrying the AGP.PAI-1 complex
    Study

    humann: not reported in source

    cultured human umbilical vein endothelial cells (HUVECs)
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The AGP.PAI-1 complex was accumulated essentially at the basal surface of endothelial cells, and such cells showed (a) morphology characteristic for strongly adhered and spread cells and (b) significantly reduced plasmin formation.
    1 context sentence
    Summary · context
    Our previous studies showed that thymosin beta4 (Tbeta4) induced the synthesis of plasminogen activator inhibitor-1 (PAI-1) in cultured human umbilical vein endothelial cells (HUVECs) via the AP-1 dependent mechanism and its enhanced secretion.
  4. 04LabIn vitro (cells)Mechanism

    In HUVECs, cells carrying the AGP.PAI-1 complex showed morphology characteristic of strongly adhered and spread cells.

    In plain wordsIn cells, those carrying the AGP.PAI-1 complex looked strongly attached and spread out.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Not applicableAdhesion and spreading of endothelial cells carrying the AGP.PAI-1 complex
    Study

    humann: not reported in source

    cultured human umbilical vein endothelial cells (HUVECs)
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The AGP.PAI-1 complex was accumulated essentially at the basal surface of endothelial cells, and such cells showed (a) morphology characteristic for strongly adhered and spread cells and (b) significantly reduced plasmin formation.

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

    13 Oct 2026, 01:52 UTC

    Study results updated

  2. Version 1

    12 Oct 2026, 18:17 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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