Thymosin Beta-4 Suppresses Osteoclastic Differentiation and Inflammatory Responses in Human Periodontal Ligament Cells.

Lee SI, Yi JK, Bae WJ, Lee S, Cha HJ, Kim EC

PloS one20 Jan 2016Cited by 23 (Europe PMC)

PMID26789270PMCIDPMC4720371DOI10.1371/journal.pone.0146708PepBankPUB-26789270

Summary

BackgroundRecent reports suggest that thymosin beta-4 (Tβ4) is a key regulator for wound healing and anti-inflammation. However, the role of Tβ4 in osteoclast differentiation remains unclear.PurposeThe purpose of this study was to evaluate Tβ4 expression in H2O2-stimulated human periodontal ligament cells (PDLCs), the effects of Tβ4 activation on inflammatory response in PDLCs and osteoclastic differentiation in mouse bone marrow-derived macrophages (BMMs), and identify the underlying mechanism.MethodsReverse transcription-polymerase chain reactions and Western blot analyses were used to measure mRNA and protein levels, respectively. Osteoclastic differentiation was assessed in mouse bone marrow-derived macrophages (BMMs) using conditioned medium (CM) from H2O2-treated PDLCs.ResultsTβ4 was down-regulated in H2O2-exposed PDLCs in dose- and time-dependent manners. Tβ4 activation with a Tβ4 peptide attenuated the H2O2-induced production of NO and PGE2 and up-regulated iNOS, COX-2, and osteoclastogenic cytokines (TNF-α, IL-1β, IL-6, IL-8, and IL-17) as well as reversed the effect on RANKL and OPG in PDLCs. Tβ4 peptide inhibited the effects of H2O2 on the activation of ERK and JNK MAPK, and NF-κB in PDLCs. Furthermore, Tβ4 peptide inhibited osteoclast differentiation, osteoclast-specific gene expression, and p38, ERK, and JNK phosphorylation and NF-κB activation in RANKL-stimulated BMMs. In addition, H2O2 up-regulated Wnt5a and its cell surface receptors, Frizzled and Ror2 in PDLCs. Wnt5a inhibition by Wnt5a siRNA enhanced the effects of Tβ4 on H2O2-mediated induction of pro-inflammatory cytokines and osteoclastogenic cytokines as well as helping osteoclastic differentiation whereas Wnt5a activation by Wnt5a peptide reversed it.ConclusionIn conclusion, this study demonstrated, for the first time, that Tβ4 was down-regulated in ROS-stimulated PDLCs as well as Tβ4 activation exhibited anti-inflammatory effects and anti-osteoclastogenesis in vitro. Thus, Tβ4 activation might be a therapeutic target for inflammatory osteolytic disease, such as periodontitis.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study9

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

01LabIn vitro (cells)Activity measurement
In H2O2-stimulated human periodontal ligament cells, Tβ4 peptide attenuated the H2O2-induced production of NO and PGE2.
In plain wordsIn cells, Tβ4 peptide reduced the nitric oxide and PGE2 made after H2O2 exposure.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseNO and PGE2 production after H2O2
Study
humann: not reported in source
human periodontal ligament cells (PDLCs)
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
Tβ4 activation with a Tβ4 peptide attenuated the H2O2-induced production of NO and PGE2 and up-regulated iNOS, COX-2, and osteoclastogenic cytokines (TNF-α, IL-1β, IL-6, IL-8, and IL-17) as well as reversed the effect on RANKL and OPG in PDLCs.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to evaluate Tβ4 expression in H2O2-stimulated human periodontal ligament cells (PDLCs), the effects of Tβ4 activation on inflammatory response in PDLCs and osteoclastic differentiation in mouse bone marrow-derived macrophages (BMMs), and identify the underlying mechanism.
Show in the study text Report a problemFND-2678927002
02LabIn vitro (cells)Activity measurement
In H2O2-stimulated human periodontal ligament cells, Tβ4 peptide changed the expression of iNOS, COX-2 and osteoclastogenic cytokines; the abstract wording on direction is ambiguous.
In plain wordsIn cells, Tβ4 peptide changed the levels of several inflammation markers. The abstract wording on direction is unclear.
Peptide
Thymosin beta-4 (human)
Outcome
MixediNOS, COX-2 and osteoclastogenic cytokines (TNF-α, IL-1β, IL-6, IL-8, IL-17)
Study
humann: not reported in source
human periodontal ligament cells (PDLCs)
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
Tβ4 activation with a Tβ4 peptide attenuated the H2O2-induced production of NO and PGE2 and up-regulated iNOS, COX-2, and osteoclastogenic cytokines (TNF-α, IL-1β, IL-6, IL-8, and IL-17) as well as reversed the effect on RANKL and OPG in PDLCs.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to evaluate Tβ4 expression in H2O2-stimulated human periodontal ligament cells (PDLCs), the effects of Tβ4 activation on inflammatory response in PDLCs and osteoclastic differentiation in mouse bone marrow-derived macrophages (BMMs), and identify the underlying mechanism.
Show in the study text Report a problemFND-2678927003
03LabIn vitro (cells)Mechanism
In H2O2-stimulated human periodontal ligament cells, Tβ4 peptide reversed the effect of H2O2 on RANKL and OPG.
In plain wordsIn cells, Tβ4 peptide reversed the changes that H2O2 caused in RANKL and OPG.
Peptide
Thymosin beta-4 (human)
Outcome
MixedRANKL and OPG effect of H2O2
Study
humann: not reported in source
human periodontal ligament cells (PDLCs)
Outcome group
Bone and joint · Musculoskeletal
Studied dose
Dose not stated
Source sentences
Summary
Tβ4 activation with a Tβ4 peptide attenuated the H2O2-induced production of NO and PGE2 and up-regulated iNOS, COX-2, and osteoclastogenic cytokines (TNF-α, IL-1β, IL-6, IL-8, and IL-17) as well as reversed the effect on RANKL and OPG in PDLCs.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to evaluate Tβ4 expression in H2O2-stimulated human periodontal ligament cells (PDLCs), the effects of Tβ4 activation on inflammatory response in PDLCs and osteoclastic differentiation in mouse bone marrow-derived macrophages (BMMs), and identify the underlying mechanism.
Show in the study text Report a problemFND-2678927004
04LabIn vitro (cells)Mechanism
In human periodontal ligament cells, Tβ4 peptide inhibited the H2O2 effects on activation of ERK and JNK MAPK and NF-κB.
In plain wordsIn cells, Tβ4 peptide blocked H2O2-driven activation of ERK, JNK and NF-κB signalling.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseERK and JNK MAPK and NF-κB activation by H2O2
Study
humann: not reported in source
human periodontal ligament cells (PDLCs)
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
Tβ4 peptide inhibited the effects of H2O2 on the activation of ERK and JNK MAPK, and NF-κB in PDLCs.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to evaluate Tβ4 expression in H2O2-stimulated human periodontal ligament cells (PDLCs), the effects of Tβ4 activation on inflammatory response in PDLCs and osteoclastic differentiation in mouse bone marrow-derived macrophages (BMMs), and identify the underlying mechanism.
Show in the study text Report a problemFND-2678927005
05LabIn vitro (cells)Activity measurement
In RANKL-stimulated mouse bone marrow-derived macrophages, Tβ4 peptide inhibited osteoclast differentiation.
In plain wordsIn mouse cells, Tβ4 peptide reduced the formation of bone-resorbing osteoclast cells.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseOsteoclast differentiation in RANKL-stimulated BMMs
Study
mousen: not reported in source
mouse bone marrow-derived macrophages (BMMs)
Outcome group
Bone and joint · Musculoskeletal
Studied dose
Dose not stated
Source sentences
Summary
Furthermore, Tβ4 peptide inhibited osteoclast differentiation, osteoclast-specific gene expression, and p38, ERK, and JNK phosphorylation and NF-κB activation in RANKL-stimulated BMMs.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to evaluate Tβ4 expression in H2O2-stimulated human periodontal ligament cells (PDLCs), the effects of Tβ4 activation on inflammatory response in PDLCs and osteoclastic differentiation in mouse bone marrow-derived macrophages (BMMs), and identify the underlying mechanism.
Show in the study text Report a problemFND-2678927006
06LabIn vitro (cells)Mechanism
In RANKL-stimulated mouse bone marrow-derived macrophages, Tβ4 peptide inhibited osteoclast-specific gene expression.
In plain wordsIn mouse cells, Tβ4 peptide lowered the activity of genes specific to osteoclasts.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseOsteoclast-specific gene expression in RANKL-stimulated BMMs
Study
mousen: not reported in source
mouse bone marrow-derived macrophages (BMMs)
Outcome group
Bone and joint · Musculoskeletal
Studied dose
Dose not stated
Source sentences
Summary
Furthermore, Tβ4 peptide inhibited osteoclast differentiation, osteoclast-specific gene expression, and p38, ERK, and JNK phosphorylation and NF-κB activation in RANKL-stimulated BMMs.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to evaluate Tβ4 expression in H2O2-stimulated human periodontal ligament cells (PDLCs), the effects of Tβ4 activation on inflammatory response in PDLCs and osteoclastic differentiation in mouse bone marrow-derived macrophages (BMMs), and identify the underlying mechanism.
Show in the study text Report a problemFND-2678927007
07LabIn vitro (cells)Mechanism
In RANKL-stimulated mouse bone marrow-derived macrophages, Tβ4 peptide inhibited p38, ERK and JNK phosphorylation and NF-κB activation.
In plain wordsIn mouse cells, Tβ4 peptide reduced signalling steps that drive osteoclast formation.
Peptide
Thymosin beta-4 (human)
Outcome
Decreasep38, ERK, JNK phosphorylation and NF-κB activation in RANKL-stimulated BMMs
Study
mousen: not reported in source
mouse bone marrow-derived macrophages (BMMs)
Outcome group
Bone and joint · Musculoskeletal
Studied dose
Dose not stated
Source sentences
Summary
Furthermore, Tβ4 peptide inhibited osteoclast differentiation, osteoclast-specific gene expression, and p38, ERK, and JNK phosphorylation and NF-κB activation in RANKL-stimulated BMMs.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to evaluate Tβ4 expression in H2O2-stimulated human periodontal ligament cells (PDLCs), the effects of Tβ4 activation on inflammatory response in PDLCs and osteoclastic differentiation in mouse bone marrow-derived macrophages (BMMs), and identify the underlying mechanism.
Show in the study text Report a problemFND-2678927008

Natural levels measured1

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

08LabEndogenous levelIn vitro (cells)Mechanism
In human periodontal ligament cells exposed to H2O2, Tβ4 expression was down-regulated in a dose- and time-dependent manner.
In plain wordsIn cells, the cells' own Tβ4 levels fell after exposure to H2O2.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseTβ4 expression in H2O2-exposed PDLCs
Study
humann: not reported in source
human periodontal ligament cells (PDLCs)
Outcome group
Inflammation markers · Immune and inflammation
Source sentences
Summary
Tβ4 was down-regulated in H2O2-exposed PDLCs in dose- and time-dependent manners.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to evaluate Tβ4 expression in H2O2-stimulated human periodontal ligament cells (PDLCs), the effects of Tβ4 activation on inflammatory response in PDLCs and osteoclastic differentiation in mouse bone marrow-derived macrophages (BMMs), and identify the underlying mechanism.
This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.
Show in the study text Report a problemFND-2678927001

Studies that did not test the peptide alone1

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).

09LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism
In H2O2-stimulated cells, Wnt5a siRNA enhanced the effects of Tβ4 on pro-inflammatory and osteoclastogenic cytokines and on osteoclastic differentiation, whereas Wnt5a peptide reversed it.
In plain wordsIn cells, blocking Wnt5a strengthened the Tβ4 effects and adding Wnt5a peptide reversed them.
Peptide
Thymosin beta-4 (human)
Outcome
MixedWnt5a modulation of Tβ4 effects on cytokines and osteoclastic differentiation
Study
humann: not reported in source
human periodontal ligament cells (PDLCs)
Outcome group
Inflammation markers · Immune and inflammation
Source sentences
Summary
Wnt5a inhibition by Wnt5a siRNA enhanced the effects of Tβ4 on H2O2-mediated induction of pro-inflammatory cytokines and osteoclastogenic cytokines as well as helping osteoclastic differentiation whereas Wnt5a activation by Wnt5a peptide reversed it.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to evaluate Tβ4 expression in H2O2-stimulated human periodontal ligament cells (PDLCs), the effects of Tβ4 activation on inflammatory response in PDLCs and osteoclastic differentiation in mouse bone marrow-derived macrophages (BMMs), and identify the underlying mechanism.
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).
Show in the study text Report a problemFND-2678927009

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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