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Study · Animal study (in vivo) · rat · 2016

9 results

Thymosin beta 4 up-regulates miR-200a expression and induces differentiation and survival of rat brain progenitor cells.

Santra M, Chopp M, Santra S, Nallani A, Vyas S, Zhang ZG, Morris DC

Journal of neurochemistry10 Nov 2015Cited by 31 (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 study9

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In rats with middle cerebral artery occlusion, exogenous Tβ4 treatment up-regulated miR-200a expression in the peri-infarct area.

    In plain wordsIn rats with stroke, Tβ4 raised miR-200a, a small regulatory RNA, in the tissue around the stroke area.

    Outcome
    IncreasemiR-200a expression in peri-infarct area
    Study

    ratn: not reported in source

    Middle cerebral artery occlusion (MCAO)
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    exogenous Tβ4 treatment up-regulated the expression of the miR-200a in vitro in rat brain progenitor cells and in vivo in the peri-infarct area of rats subjected to middle cerebral artery occlusion (MCAO)
  2. 02AnimalAnimal study (in vivo)Mechanism

    In rat progenitor cells and MCAO rats, miR-200a up-regulation by Tβ4 down-regulated expression of Grb2.

    In plain wordsIn rat brain cells and stroke rats, the Tβ4 effect on miR-200a lowered Grb2, a protein that blocks myelin protein production.

    Outcome
    DecreaseGrb2 expression
    Study

    ratn: not reported in source

    Rat brain progenitor cells and MCAO
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The up-regulation of miR-200a down-regulated the expression of the following targets in vitro and in vivo models: (i) growth factor receptor-bound protein 2 (Grb2)
  3. 03AnimalAnimal study (in vivo)Mechanism

    In rat progenitor cells and MCAO rats, miR-200a up-regulation by Tβ4 down-regulated ERRFI-1/Mig-6, which resulted in EGFR activation/phosphorylation.

    In plain wordsIn rat brain cells and stroke rats, the Tβ4 effect on miR-200a lowered Mig-6 and activated EGFR, a growth signal receptor.

    Outcome
    DecreaseERRFI-1/Mig-6 expression and EGFR phosphorylation
    Study

    ratn: not reported in source

    Rat brain progenitor cells and MCAO
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    (ii) ERRFI-1/Mig-6, an endogenous potent kinase inhibitor of EGFR, which resulted in activation/phosphorylation of EGFR
    1 context sentence
    Summary · context
    The up-regulation of miR-200a down-regulated the expression of the following targets in vitro and in vivo models
  4. 04AnimalAnimal study (in vivo)Mechanism

    In rat progenitor cells and MCAO rats, miR-200a up-regulation by Tβ4 down-regulated friend of GATA 2 and PTEN, which resulted in marked AKT activation.

    In plain wordsIn rat brain cells and stroke rats, the Tβ4 effect on miR-200a lowered FOG2 and PTEN and strongly activated AKT, a cell survival signal.

    Outcome
    DecreaseFOG2 and PTEN expression and AKT activation
    Study

    ratn: not reported in source

    Rat brain progenitor cells and MCAO
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    (iii) friend of GATA 2, and phosphatase and tensin homolog deleted in chromosome 10 (PTEN), which are potent inhibitors of the phosphatidylinositol-3-kinase (PI3K)/AKT signaling pathway, and resulted in marked activation of AKT
    1 context sentence
    Summary · context
    The up-regulation of miR-200a down-regulated the expression of the following targets in vitro and in vivo models
  5. 05AnimalAnimal study (in vivo)Mechanism

    In rat progenitor cells and MCAO rats, miR-200a up-regulation by Tβ4 down-regulated p53, and possibly reduced apoptosis of progenitor cells under oxygen glucose deprivation.

    In plain wordsIn rat brain cells and stroke rats, the Tβ4 effect on miR-200a lowered p53, a protein that triggers cell death.

    Outcome
    Decreasep53 expression
    Study

    ratn: not reported in source

    Rat brain progenitor cells and MCAO
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    (iv) transcription factor, p53, which induces pro-apoptotic genes, and possibly reduced apoptosis of the progenitor cells subjected to oxygen glucose deprivation (OGD)
    1 context sentence
    Summary · context
    The up-regulation of miR-200a down-regulated the expression of the following targets in vitro and in vivo models
  6. 06LabIn vitro (cells)Mechanism

    In rat brain progenitor cells in vitro, exogenous Tβ4 treatment up-regulated miR-200a expression.

    In plain wordsIn rat brain cells in the lab, Tβ4 raised the level of miR-200a, a small regulatory RNA.

    Outcome
    IncreasemiR-200a expression in progenitor cells
    Study

    ratn: not reported in source

    Rat brain progenitor cells
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    exogenous Tβ4 treatment up-regulated the expression of the miR-200a in vitro in rat brain progenitor cells
  7. 07LabIn vitro (cells)Mechanism

    In rat brain progenitor cells in vitro, Tβ4 up-regulated myelin basic protein synthesis in a miR-200a dependent way.

    In plain wordsIn rat brain cells in the lab, Tβ4 increased production of myelin basic protein, a marker of mature myelin-forming cells.

    Outcome
    IncreaseMyelin basic protein synthesis
    Study

    ratn: not reported in source

    Rat brain progenitor cells
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Tβ4 up-regulated MBP synthesis, and inhibited OGD-induced apoptosis in a novel miR-200a dependent EGFR signaling pathway
  8. 08LabIn vitro (cells)Mechanism

    In rat brain progenitor cells in vitro, Tβ4 inhibited apoptosis induced by oxygen glucose deprivation in a miR-200a dependent way.

    In plain wordsIn rat brain cells in the lab, Tβ4 reduced cell death caused by lack of oxygen and glucose.

    Outcome
    DecreaseOGD-induced apoptosis
    Study

    ratn: not reported in source

    Rat brain progenitor cells under oxygen glucose deprivation
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    inhibited OGD-induced apoptosis in a novel miR-200a dependent EGFR signaling pathway
  9. 09LabIn vitro (cells)Mechanism

    In rat brain progenitor cells in vitro, anti-miR-200a transfection reversed all the effects of Tβ4 treatment.

    In plain wordsIn rat brain cells in the lab, blocking miR-200a cancelled all the effects of Tβ4.

    Outcome
    Not applicableEffect of anti-miR-200a on Tβ4 treatment effects
    Study

    ratn: not reported in source

    Rat brain progenitor cells
    Comparator
    Tβ4 without anti-miR-200a
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Anti-miR-200a transfection reversed all the effects of Tβ4 treatment in vitro.

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

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