Thymosin Beta 4 Protects Hippocampal Neuronal Cells against PrP (106-126) via Neurotrophic Factor Signaling.

Kim S, Choi J, Kwon J

Molecules (Basel, Switzerland)6 May 2023

PMID37175330PMCIDPMC10180446DOI10.3390/molecules28093920PepBankPUB-37175330

Summary

Prion protein peptide (PrP) has demonstrated neurotoxicity in brain cells, resulting in the progression of prion diseases with spongiform degenerative, amyloidogenic, and aggregative properties. Thymosin beta 4 (Tβ₄) plays a role in the nervous system and may be related to motility, axonal enlargement, differentiation, neurite outgrowth, and proliferation. However, no studies about the effects of Tβ₄ on prion disease have been performed yet. In the present study, we investigated the protective effect of Tβ₄ against synthetic PrP (106-126) and considered possible mechanisms. Hippocampal neuronal HT22 cells were treated with Tβ₄ and PrP (106-126) for 24 h. Tβ₄ significantly reversed cell viability and reactive oxidative species (ROS) affected by PrP (106-126). Apoptotic proteins induced by PrP (106-126) were reduced by Tβ₄. Interestingly, a balance of neurotrophic factors (nerve growth factor and brain-derived neurotrophic factor) and receptors (nerve growth factor receptor p75, tropomyosin related kinase A and B) were competitively maintained by Tβ₄ through receptors reacting to PrP (106-126). Our results demonstrate that Tβ₄ protects neuronal cells against PrP (106-126) neurotoxicity via the interaction of neurotrophic factors/receptors.

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.

01LabIn vitro (cells)Efficacy outcome
In HT22 hippocampal neuronal cells, Tβ4 reversed the loss of cell viability caused by PrP (106-126).
In plain wordsIn cells, thymosin β4 protected nerve cells from a toxic prion peptide and kept more of them alive.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseCell viability against PrP (106-126)
Study
n: not reported in source
HT22 hippocampal neuronal cells
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated · 24 hAs given in this study.
Source sentences
Summary
Tβ₄ significantly reversed cell viability and reactive oxidative species (ROS) affected by PrP (106-126).
1 context sentence(design, population, supporting numbers)
Summary · context
Hippocampal neuronal HT22 cells were treated with Tβ₄ and PrP (106-126) for 24 h.
Show in the study text Report a problemFND-3717533001
02LabIn vitro (cells)Efficacy outcome
In HT22 hippocampal neuronal cells, Tβ4 reversed the rise in reactive oxygen species caused by PrP (106-126).
In plain wordsIn cells, thymosin β4 lowered the oxidative stress that a toxic prion peptide caused in nerve cells.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseReactive oxygen species against PrP (106-126)
Study
n: not reported in source
HT22 hippocampal neuronal cells
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated · 24 hAs given in this study.
Source sentences
Summary
Tβ₄ significantly reversed cell viability and reactive oxidative species (ROS) affected by PrP (106-126).
1 context sentence(design, population, supporting numbers)
Summary · context
Hippocampal neuronal HT22 cells were treated with Tβ₄ and PrP (106-126) for 24 h.
Show in the study text Report a problemFND-3717533002
03LabIn vitro (cells)Mechanism
In HT22 hippocampal neuronal cells, Tβ4 reduced apoptotic proteins induced by PrP (106-126).
In plain wordsIn cells, thymosin β4 lowered cell-death proteins that a toxic prion peptide raised in nerve cells.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseApoptotic proteins induced by PrP (106-126)
Study
n: not reported in source
HT22 hippocampal neuronal cells
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated · 24 hAs given in this study.
Source sentences
Summary
Apoptotic proteins induced by PrP (106-126) were reduced by Tβ₄.
1 context sentence(design, population, supporting numbers)
Summary · context
Hippocampal neuronal HT22 cells were treated with Tβ₄ and PrP (106-126) for 24 h.
Show in the study text Report a problemFND-3717533003
04LabIn vitro (cells)Mechanism
In HT22 hippocampal neuronal cells exposed to PrP (106-126), Tβ4 maintained the balance of neurotrophic factors (NGF, BDNF) and their receptors (p75, TrkA, TrkB).
In plain wordsIn cells, thymosin β4 kept growth factors and their receptors in balance when nerve cells met a toxic prion peptide.
Peptide
Thymosin beta-4 (human)
Outcome
Not applicableNeurotrophic factor and receptor balance
Study
n: not reported in source
HT22 hippocampal neuronal cells
Outcome group
Neuroprotection · Nervous system and cognition
Studied dose
Dose not stated · 24 hAs given in this study.
Source sentences
Summary
Interestingly, a balance of neurotrophic factors (nerve growth factor and brain-derived neurotrophic factor) and receptors (nerve growth factor receptor p75, tropomyosin related kinase A and B) were competitively maintained by Tβ₄ through receptors reacting to PrP (106-126).
1 context sentence(design, population, supporting numbers)
Summary · context
Hippocampal neuronal HT22 cells were treated with Tβ₄ and PrP (106-126) for 24 h.
Show in the study text Report a problemFND-3717533004

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.

Version 2Current
13 Oct 2026, 01:52 UTC
Study results updated
Version 1
12 Oct 2026, 18:17 UTC
First added · source update from Europe PMC

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