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Study · In vitro (cells) · 2009

6 results

Thymosin beta4 induces endothelial progenitor cell migration via PI3K/Akt/eNOS signal transduction pathway.

Qiu FY, Song XX, Zheng H, Zhao YB, Fu GS

Journal of cardiovascular pharmacology1 Mar 2009Cited by 44 (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 study6

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

  1. 01LabIn vitro (cells)Activity measurement

    In endothelial progenitor cells, thymosin beta4 increased migration in a concentration-dependent manner.

    In plain wordsIn cells, thymosin beta4 made endothelial progenitor cells migrate more, with a larger effect at higher concentrations.

    Outcome
    IncreaseEPC migration in transwell assay
    Study

    n: not reported in source

    Endothelial progenitor cells
    Outcome group
    Angiogenesis · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In our study, using a transwell migration assay, we showed that thymosin beta4 induced EPC migration in a concentration-dependent manner.
  2. 02LabIn vitro (cells)Mechanism

    In endothelial progenitor cells, thymosin beta4 increased Akt phosphorylation in a time- and concentration-dependent manner.

    In plain wordsIn cells, thymosin beta4 increased Akt activation over time and with higher concentration.

    Outcome
    IncreaseAkt phosphorylation
    Study

    n: not reported in source

    Endothelial progenitor cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Western blot analysis revealed that treatment of EPCs with thymosin beta4 resulted in a time and concentration-dependent phosphorylation of Akt, endothelial nitric oxide synthase (eNOS), and extracellular signal-regulated kinase (ERK)1/2.
  3. 03LabIn vitro (cells)Mechanism

    In endothelial progenitor cells, thymosin beta4 increased eNOS phosphorylation in a time- and concentration-dependent manner.

    In plain wordsIn cells, thymosin beta4 increased eNOS activation over time and with higher concentration.

    Outcome
    IncreaseeNOS phosphorylation
    Study

    n: not reported in source

    Endothelial progenitor cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Western blot analysis revealed that treatment of EPCs with thymosin beta4 resulted in a time and concentration-dependent phosphorylation of Akt, endothelial nitric oxide synthase (eNOS), and extracellular signal-regulated kinase (ERK)1/2.
  4. 04LabIn vitro (cells)Mechanism

    In endothelial progenitor cells, thymosin beta4 increased ERK1/2 phosphorylation in a time- and concentration-dependent manner.

    In plain wordsIn cells, thymosin beta4 increased ERK1/2 activation over time and with higher concentration.

    Outcome
    IncreaseERK1/2 phosphorylation
    Study

    n: not reported in source

    Endothelial progenitor cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Western blot analysis revealed that treatment of EPCs with thymosin beta4 resulted in a time and concentration-dependent phosphorylation of Akt, endothelial nitric oxide synthase (eNOS), and extracellular signal-regulated kinase (ERK)1/2.

Studies that did not test the peptide alone2

In this study, Thymosin beta-4 (human) 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 Thymosin beta-4 (human).

  1. 05LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In endothelial progenitor cells, PI3K inhibitors or an eNOS inhibitor blocked the migration that thymosin beta4 induced.

    In plain wordsIn cells, drugs that block PI3K or eNOS stopped the extra cell movement caused by thymosin beta4.

    Outcome
    DecreaseThymosin beta4-induced migration with PI3K or eNOS inhibitors
    Study

    n: not reported in source

    Endothelial progenitor cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    Functional analysis showed that thymosin beta4-induced EPC migration was blocked by phosphatidylinositol 3-kinase inhibitors (LY294002 or wortmannin) or eNOS inhibitor (Nomega-nitro-L-arginine methyl ester)

    In this study, Thymosin beta-4 (human) 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 Thymosin beta-4 (human).

  2. 06LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In endothelial progenitor cells, a MAPK/ERK inhibitor did not significantly attenuate thymosin beta4-induced migration.

    In plain wordsIn cells, a drug that blocks MAPK/ERK did not clearly reduce the cell movement caused by thymosin beta4.

    Outcome
    No significant changeThymosin beta4-induced migration with MAPK/ERK inhibitor
    Study

    n: not reported in source

    Endothelial progenitor cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    but was not significantly attenuated by mitogen-activated protein kinase (MAPK)/ERK inhibitor (PD98059).

    In this study, Thymosin beta-4 (human) 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 Thymosin beta-4 (human).

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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