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Study · In vitro (cells) · 2025

2 results

Thymosin β4 stabilizes hypoxia induced brain microvascular endothelial cell dysfunction through S1PR1 dependent mechanisms.

Stewart WG, Hejl CD, Guleria RS, Gupta S

Scientific reports1 Dec 2025Cited by 3 (Europe PMC)

PMID41326489 (opens in a new tab)PMCIDPMC12756306 (opens in a new tab)DOI10.1038/s41598-025-28435-2 (opens in a new tab)PepBankPUB-41326489
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Summary

Acute ischemic injury causes impairment of blood brain barrier (BBB) permeability and is considered as secondary insult in the brain after traumatic brain injury (TBI). The mechanisms underlying these events are incomprehensible and therefore therapeutic opportunities are limited. Although drugs have been showing some promise in TBI outcome, the restoration of BBB damage remain elusive. Thymosin β4 (Tβ4) is a secreted 43 amino acid peptide showed beneficial outcome in cerebral ischemia or TBI, however, it's role in hypoxia-induced BBB damage remains elusive. We hypothesize that Tβ4 protect hypoxia-induced BBB disruption via Sphingosine 1-phosphate receptor 1 (S1PR1) modulation. In the current study, we investigated the beneficial effects of Tβ4 in hypoxia induced gene expression of several tight junction proteins, S1PR1, endothelial cell permeability and tight junction dynamics in human brain microvascular endothelial cells (hBMVECs), one of the important cell types in the BBB integrity. The data suggests that pretreatment with Tβ4 reversed the hypoxia-induced damage of BBB components in hBMVECs. Furthermore, results identify S1PR1, a possible target for Tβ4. Inhibition of S1PR1 showed that Tβ4 failed to offer protection. Together, data provided evidence that S1PR1 is pivotal and Tβ4 can serve as a protective agent in BBB integrity and may offer a promising therapeutic target. In conclusion, we propose that depletion of S1PR1signaling is vital in hypoxia-induced BBB pathophysiology and Tβ4 may be tested as a potential treatment modality and warrant further investigation.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study2

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In human brain microvascular endothelial cells, pretreatment with Tβ4 reversed the hypoxia-induced damage of blood brain barrier components.

    In plain wordsIn cells, Tβ4 given before low oxygen reversed damage to the blood brain barrier components.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseHypoxia-induced damage of BBB components
    Study

    humann: not reported in source

    Human brain microvascular endothelial cells (hBMVECs) under hypoxia
    Comparator
    Hypoxia without Tβ4
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The data suggests that pretreatment with Tβ4 reversed the hypoxia-induced damage of BBB components in hBMVECs.
    1 context sentence
    Summary · context
    In the current study, we investigated the beneficial effects of Tβ4 in hypoxia induced gene expression of several tight junction proteins, S1PR1, endothelial cell permeability and tight junction dynamics in human brain microvascular endothelial cells (hBMVECs), one of the important cell types in the BBB integrity.
  2. 02LabIn vitro (cells)Mechanism

    In human brain microvascular endothelial cells under hypoxia, Tβ4 failed to offer protection when S1PR1 was inhibited.

    In plain wordsIn cells, Tβ4 did not protect against low oxygen damage when its possible target S1PR1 was blocked.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    No significant changeTβ4 protection after S1PR1 inhibition
    Study

    humann: not reported in source

    Human brain microvascular endothelial cells (hBMVECs) under hypoxia
    Comparator
    Hypoxia without Tβ4
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Inhibition of S1PR1 showed that Tβ4 failed to offer protection.
    1 context sentence
    Summary · context
    In the current study, we investigated the beneficial effects of Tβ4 in hypoxia induced gene expression of several tight junction proteins, S1PR1, endothelial cell permeability and tight junction dynamics in human brain microvascular endothelial cells (hBMVECs), one of the important cell types in the BBB integrity.

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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