Thymosin beta-4 improves endothelial function and reparative potency of diabetic endothelial cells differentiated from patient induced pluripotent stem cells.

Su L, Kong X, Loo S, Gao Y, Liu B, Su X, Dalan R, Ma J, Ye L

Stem cell research & therapy10 Jan 2022Cited by 15 (Europe PMC)

PMID35012642PMCIDPMC8751378DOI10.1186/s13287-021-02687-xPepBankPUB-35012642

Summary

BackgroundPrior studies show that signature phenotypes of diabetic human induced pluripotent stem cells derived endothelial cells (dia-hiPSC-ECs) are disrupted glycine homeostasis, increased senescence, impaired mitochondrial function and angiogenic potential as compared with healthy hiPSC-ECs. In the current study, we aimed to assess the role of thymosin β-4 (Tb-4) on endothelial function using dia-hiPSC-ECs as disease model of endothelial dysfunction.Methods and resultsUsing dia-hiPSC-ECs as models of endothelial dysfunction, we determined the effect of Tb-4 on cell proliferation, senescence, cyto-protection, protein expression of intercellular adhesion molecule-1 (ICAM-1), secretion of endothelin-1 and MMP-1, mitochondrial membrane potential, and cyto-protection in vitro and angiogenic potential for treatment of ischemic limb disease in a mouse model of type 2 diabetes mellitus (T2DM) in vivo. We found that 600 ng/mL Tb4 significantly up-regulated AKT activity and Bcl-XL protein expression, enhanced dia-hiPSC-EC viability and proliferation, limited senescence, reduced endothelin-1 and MMP-1 secretion, and improved reparative potency of dia-hiPSC-ECs for treatment of ischemic limb disease in mice with T2DM. However, Tb4 had no effect on improving mitochondrial membrane potential and glycine homeostasis and reducing intercellular adhesion molecule-1 protein expression in dia-hiPSC-ECs.ConclusionsTb-4 improves endothelial dysfunction through enhancing hiPSC-EC viability, reducing senescence and endothelin-1 production, and improves angiogenic potency in diabetes.

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

Results from this study11

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

01AnimalAnimal study (in vivo)Efficacy outcome
In mice with type 2 diabetes and ischemic limb disease, Tb4 improved the reparative potency of dia-hiPSC-ECs.
In plain wordsIn diabetic mice with limb ischemia, Tb4 improved the repair effect of lab-grown endothelial cells.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseReparative potency of dia-hiPSC-ECs in ischemic limb disease
Study
mousen: not reported in source
type 2 diabetes mouse model of ischemic limb disease
Outcome group
Angiogenesis · Cardiovascular
Studied dose
Dose not stated
Source sentences
Summary
improved reparative potency of dia-hiPSC-ECs for treatment of ischemic limb disease in mice with T2DM.
1 context sentence(design, population, supporting numbers)
Summary · context
and angiogenic potential for treatment of ischemic limb disease in a mouse model of type 2 diabetes mellitus (T2DM) in vivo.
Show in the study text Report a problemFND-3501264208
02LabIn vitro (cells)Mechanism
In diabetic hiPSC-derived endothelial cells, 600 ng/mL Tb4 significantly up-regulated AKT activity.
In plain wordsIn lab-grown endothelial cells that model diabetes, Tb4 raised AKT activity.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseAKT activity
Study
humann: not reported in source
diabetic hiPSC-derived endothelial cells (dia-hiPSC-ECs)
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
600 ng/mLAs given in this study (human).
Source sentences
Summary
We found that 600 ng/mL Tb4 significantly up-regulated AKT activity and Bcl-XL protein expression, enhanced dia-hiPSC-EC viability and proliferation, limited senescence, reduced endothelin-1 and MMP-1 secretion, and improved reparative potency of dia-hiPSC-ECs for treatment of ischemic limb disease in mice with T2DM.
Show in the study text Report a problemFND-3501264201
03LabIn vitro (cells)Mechanism
In diabetic hiPSC-derived endothelial cells, 600 ng/mL Tb4 significantly up-regulated Bcl-XL protein expression.
In plain wordsIn lab-grown endothelial cells that model diabetes, Tb4 raised Bcl-XL protein.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseBcl-XL protein expression
Study
humann: not reported in source
diabetic hiPSC-derived endothelial cells (dia-hiPSC-ECs)
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
600 ng/mLAs given in this study (human).
Source sentences
Summary
We found that 600 ng/mL Tb4 significantly up-regulated AKT activity and Bcl-XL protein expression, enhanced dia-hiPSC-EC viability and proliferation, limited senescence, reduced endothelin-1 and MMP-1 secretion, and improved reparative potency of dia-hiPSC-ECs for treatment of ischemic limb disease in mice with T2DM.
Show in the study text Report a problemFND-3501264202
04LabIn vitro (cells)Efficacy outcome
In diabetic hiPSC-derived endothelial cells, 600 ng/mL Tb4 enhanced cell viability.
In plain wordsIn lab-grown endothelial cells that model diabetes, Tb4 improved cell viability.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseCell viability
Study
humann: not reported in source
diabetic hiPSC-derived endothelial cells (dia-hiPSC-ECs)
Outcome group
Cell proliferation and differentiation · Cardiovascular
Studied dose
600 ng/mLAs given in this study (human).
Source sentences
Summary
We found that 600 ng/mL Tb4 significantly up-regulated AKT activity and Bcl-XL protein expression, enhanced dia-hiPSC-EC viability and proliferation, limited senescence, reduced endothelin-1 and MMP-1 secretion, and improved reparative potency of dia-hiPSC-ECs for treatment of ischemic limb disease in mice with T2DM.
Show in the study text Report a problemFND-3501264203
05LabIn vitro (cells)Efficacy outcome
In diabetic hiPSC-derived endothelial cells, 600 ng/mL Tb4 enhanced cell proliferation.
In plain wordsIn lab-grown endothelial cells that model diabetes, Tb4 increased cell growth.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseCell proliferation
Study
humann: not reported in source
diabetic hiPSC-derived endothelial cells (dia-hiPSC-ECs)
Outcome group
Cell proliferation and differentiation · Cardiovascular
Studied dose
600 ng/mLAs given in this study (human).
Source sentences
Summary
We found that 600 ng/mL Tb4 significantly up-regulated AKT activity and Bcl-XL protein expression, enhanced dia-hiPSC-EC viability and proliferation, limited senescence, reduced endothelin-1 and MMP-1 secretion, and improved reparative potency of dia-hiPSC-ECs for treatment of ischemic limb disease in mice with T2DM.
Show in the study text Report a problemFND-3501264204
06LabIn vitro (cells)Efficacy outcome
In diabetic hiPSC-derived endothelial cells, 600 ng/mL Tb4 limited senescence.
In plain wordsIn lab-grown endothelial cells that model diabetes, Tb4 limited cell aging.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseSenescence
Study
humann: not reported in source
diabetic hiPSC-derived endothelial cells (dia-hiPSC-ECs)
Outcome group
Aging markers · Cardiovascular
Studied dose
600 ng/mLAs given in this study (human).
Source sentences
Summary
We found that 600 ng/mL Tb4 significantly up-regulated AKT activity and Bcl-XL protein expression, enhanced dia-hiPSC-EC viability and proliferation, limited senescence, reduced endothelin-1 and MMP-1 secretion, and improved reparative potency of dia-hiPSC-ECs for treatment of ischemic limb disease in mice with T2DM.
Show in the study text Report a problemFND-3501264205
07LabIn vitro (cells)Efficacy outcome
In diabetic hiPSC-derived endothelial cells, 600 ng/mL Tb4 reduced endothelin-1 secretion.
In plain wordsIn lab-grown endothelial cells that model diabetes, Tb4 lowered endothelin-1 release.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseEndothelin-1 secretion
Study
humann: not reported in source
diabetic hiPSC-derived endothelial cells (dia-hiPSC-ECs)
Outcome group
Lung injury and fibrosis · Cardiovascular
Studied dose
600 ng/mLAs given in this study (human).
Source sentences
Summary
We found that 600 ng/mL Tb4 significantly up-regulated AKT activity and Bcl-XL protein expression, enhanced dia-hiPSC-EC viability and proliferation, limited senescence, reduced endothelin-1 and MMP-1 secretion, and improved reparative potency of dia-hiPSC-ECs for treatment of ischemic limb disease in mice with T2DM.
Show in the study text Report a problemFND-3501264206
08LabIn vitro (cells)Efficacy outcome
In diabetic hiPSC-derived endothelial cells, 600 ng/mL Tb4 reduced MMP-1 secretion.
In plain wordsIn lab-grown endothelial cells that model diabetes, Tb4 lowered MMP-1 release.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseMMP-1 secretion
Study
humann: not reported in source
diabetic hiPSC-derived endothelial cells (dia-hiPSC-ECs)
Outcome group
Lung injury and fibrosis · Cardiovascular
Studied dose
600 ng/mLAs given in this study (human).
Source sentences
Summary
We found that 600 ng/mL Tb4 significantly up-regulated AKT activity and Bcl-XL protein expression, enhanced dia-hiPSC-EC viability and proliferation, limited senescence, reduced endothelin-1 and MMP-1 secretion, and improved reparative potency of dia-hiPSC-ECs for treatment of ischemic limb disease in mice with T2DM.
Show in the study text Report a problemFND-3501264207
09LabIn vitro (cells)Efficacy outcome
In diabetic hiPSC-derived endothelial cells, Tb4 had no effect on mitochondrial membrane potential.
In plain wordsIn lab-grown endothelial cells that model diabetes, Tb4 did not change mitochondrial membrane potential.
Peptide
Thymosin beta-4 (human)
Outcome
No significant changeMitochondrial membrane potential
Study
humann: not reported in source
diabetic hiPSC-derived endothelial cells (dia-hiPSC-ECs)
Outcome group
Mitochondrial function · Cardiovascular
Studied dose
600 ng/mLAs given in this study (human).
Source sentences
Summary
However, Tb4 had no effect on improving mitochondrial membrane potential and glycine homeostasis and reducing intercellular adhesion molecule-1 protein expression in dia-hiPSC-ECs.
Show in the study text Report a problemFND-3501264209
10LabIn vitro (cells)Efficacy outcome
In diabetic hiPSC-derived endothelial cells, Tb4 had no effect on improving glycine homeostasis.
In plain wordsIn lab-grown endothelial cells that model diabetes, Tb4 did not improve glycine balance.
Peptide
Thymosin beta-4 (human)
Outcome
No significant changeGlycine homeostasis
Study
humann: not reported in source
diabetic hiPSC-derived endothelial cells (dia-hiPSC-ECs)
Outcome group
Lung injury and fibrosis · Cardiovascular
Studied dose
600 ng/mLAs given in this study (human).
Source sentences
Summary
However, Tb4 had no effect on improving mitochondrial membrane potential and glycine homeostasis and reducing intercellular adhesion molecule-1 protein expression in dia-hiPSC-ECs.
Show in the study text Report a problemFND-3501264210
11LabIn vitro (cells)Efficacy outcome
In diabetic hiPSC-derived endothelial cells, Tb4 had no effect on reducing ICAM-1 protein expression.
In plain wordsIn lab-grown endothelial cells that model diabetes, Tb4 did not lower ICAM-1 protein.
Peptide
Thymosin beta-4 (human)
Outcome
No significant changeICAM-1 protein expression
Study
humann: not reported in source
diabetic hiPSC-derived endothelial cells (dia-hiPSC-ECs)
Outcome group
Inflammation markers · Cardiovascular
Studied dose
600 ng/mLAs given in this study (human).
Source sentences
Summary
However, Tb4 had no effect on improving mitochondrial membrane potential and glycine homeostasis and reducing intercellular adhesion molecule-1 protein expression in dia-hiPSC-ECs.
Show in the study text Report a problemFND-3501264211

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

Subjects

Terms as the source lists them.

Publication types

MeSH terms

Keywords

PepBank is a research reference. Talk to a doctor before you use any peptide.