Systemic gene therapy with thymosin β4 alleviates glomerular injury in mice.

Mason WJ, Jafree DJ, Pomeranz G, Kolatsi-Joannou M, Rottner AK, Pacheco S, Moulding DA, Wolf A, Kupatt C, Peppiatt-Wildman C, Papakrivopoulou E, Riley PR, Long DA, Vasilopoulou E

Scientific reports16 Jul 2022Cited by 9 (Europe PMC)

PMID35842494DOI10.1038/s41598-022-16287-zPepBankPUB-35842494

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Summary

Plasma ultrafiltration in the kidney occurs across glomerular capillaries, which are surrounded by epithelial cells called podocytes. Podocytes have a unique shape maintained by a complex cytoskeleton, which becomes disrupted in glomerular disease resulting in defective filtration and albuminuria. Lack of endogenous thymosin β4 (TB4), an actin sequestering peptide, exacerbates glomerular injury and disrupts the organisation of the podocyte actin cytoskeleton, however, the potential of exogenous TB4 therapy to improve podocyte injury is unknown. Here, we have used Adriamycin (ADR), a toxin which injures podocytes and damages the glomerular filtration barrier leading to albuminuria in mice. Through interrogating single-cell RNA-sequencing data of isolated glomeruli we demonstrate that ADR injury results in reduced levels of podocyte TB4. Administration of an adeno-associated viral vector encoding TB4 increased the circulating level of TB4 and prevented ADR-induced podocyte loss and albuminuria. ADR injury was associated with disorganisation of the podocyte actin cytoskeleton in vitro, which was ameliorated by treatment with exogenous TB4. Collectively, we propose that systemic gene therapy with TB4 prevents podocyte injury and maintains glomerular filtration via protection of the podocyte cytoskeleton thus presenting a novel treatment strategy for glomerular disease.

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

Results from this study5

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

01LabIn vitro (cells)Efficacy outcome
In podocytes injured by Adriamycin in vitro, exogenous TB4 ameliorated the disorganisation of the actin cytoskeleton.
In plain wordsIn cells, added TB4 reduced the disorganisation of the podocyte actin skeleton caused by Adriamycin injury.
Peptide
Thymosin beta-4 (human)
Outcome
IncreasePodocyte actin cytoskeleton organisation
Study
n: not reported in source
podocytes with ADR injury in vitro
Outcome group
Kidney function · Kidney and urinary
Studied dose
Dose not stated
Source sentences
Summary
ADR injury was associated with disorganisation of the podocyte actin cytoskeleton in vitro, which was ameliorated by treatment with exogenous TB4.
1 context sentence(design, population, supporting numbers)
Summary · context
Here, we have used Adriamycin (ADR), a toxin which injures podocytes and damages the glomerular filtration barrier leading to albuminuria in mice.
Show in the study text Report a problemFND-3584249405

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.

02AnimalEndogenous levelAnimal study (in vivo)Mechanism
In mice, Adriamycin injury reduced the level of the body's own TB4 in podocytes, as seen in single-cell RNA-sequencing data of isolated glomeruli.
In plain wordsIn mice, kidney injury lowered the body's own TB4 levels in podocytes.
Peptide
Thymosin beta-4 (human)
Outcome
DecreasePodocyte TB4 level after ADR injury
Study
mousen: not reported in source
Adriamycin-induced glomerular injury
Outcome group
Kidney function · Kidney and urinary
Source sentences
Summary
Through interrogating single-cell RNA-sequencing data of isolated glomeruli we demonstrate that ADR injury results in reduced levels of podocyte TB4.
1 context sentence(design, population, supporting numbers)
Summary · context
Here, we have used Adriamycin (ADR), a toxin which injures podocytes and damages the glomerular filtration barrier leading to albuminuria in mice.
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-3584249401

Studies that did not test the peptide alone3

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).

03AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Pharmacokinetics
In mice, an adeno-associated viral vector encoding TB4 increased the circulating level of TB4.
In plain wordsIn mice, a virus that carries the Tβ4 gene raised the Tβ4 level in the blood.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseCirculating TB4 level after AAV-TB4
Study
mousen: not reported in source
Adriamycin-induced glomerular injury
Outcome group
Pharmacokinetics · Pharmacology
Source sentences
Summary
Administration of an adeno-associated viral vector encoding TB4 increased the circulating level of TB4
1 context sentence(design, population, supporting numbers)
Summary · context
Here, we have used Adriamycin (ADR), a toxin which injures podocytes and damages the glomerular filtration barrier leading to albuminuria in mice.
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-3584249402
04AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Efficacy outcome
In mice with Adriamycin-induced glomerular injury, AAV-TB4 gene therapy prevented podocyte loss.
In plain wordsIn mice with kidney filter injury, a virus that carries the Tβ4 gene prevented the loss of podocytes, the kidney filter cells.
Peptide
Thymosin beta-4 (human)
Outcome
DecreasePodocyte loss after ADR injury
Study
mousen: not reported in source
Adriamycin-induced glomerular injury
Outcome group
Kidney function · Kidney and urinary
Source sentences
Summary
Administration of an adeno-associated viral vector encoding TB4 increased the circulating level of TB4 and prevented ADR-induced podocyte loss and albuminuria.
1 context sentence(design, population, supporting numbers)
Summary · context
Here, we have used Adriamycin (ADR), a toxin which injures podocytes and damages the glomerular filtration barrier leading to albuminuria in mice.
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-3584249403
05AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Efficacy outcome
In mice with Adriamycin-induced glomerular injury, AAV-TB4 gene therapy prevented albuminuria.
In plain wordsIn mice with kidney filter injury, a virus that carries the Tβ4 gene prevented protein leaking into the urine.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseAlbuminuria after ADR injury
Study
mousen: not reported in source
Adriamycin-induced glomerular injury
Outcome group
Kidney function · Kidney and urinary
Source sentences
Summary
Administration of an adeno-associated viral vector encoding TB4 increased the circulating level of TB4 and prevented ADR-induced podocyte loss and albuminuria.
1 context sentence(design, population, supporting numbers)
Summary · context
Here, we have used Adriamycin (ADR), a toxin which injures podocytes and damages the glomerular filtration barrier leading to albuminuria in mice.
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-3584249404

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

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