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Study · Measured the body's own peptide · 2005

3 results

Proteomic patterns and prediction of glomerulosclerosis and its mechanisms.

Xu BJ, Shyr Y, Liang X, Ma LJ, Donnert EM, Roberts JD, Zhang X, Kon V, Brown NJ, Caprioli RM, Fogo AB

Journal of the American Society of Nephrology : JASN3 Aug 2005Cited by 85 (Europe PMC)

PMID16079267 (opens in a new tab)DOI10.1681/asn.2005030262 (opens in a new tab)PepBankPUB-16079267
Publisher pagePubMedAsk about this study
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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 study3

No result from this study comes from a test of the peptide.

Natural levels measured2

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.

  1. 01AnimalEndogenous levelAnimal study (in vivo)Mechanism

    In rats with 5/6 nephrectomy, proteomic profiling identified thymosin beta4 as a key differentially expressed protein in glomeruli.

    In plain wordsIn rats with kidney damage, the body's own thymosin beta4 was a key protein that differed in the kidney filters.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Direction not reportedThymosin beta4 as differentially expressed protein in glomeruli
    Study

    ratn: not reported in source

    5/6 nephrectomy model of focal segmental glomerulosclerosis
    Outcome group
    Kidney function · Kidney and urinary

    Source sentences

    Summary
    Thymosin beta4, a protein with relevant interactions with plasminogen activator inhibitor-1, angiogenesis, and wound healing, was identified as a key differentially expressed protein.
    2 context sentences
    Summary · context
    Protein expression profiles linked to sclerosis in the 5/6 nephrectomy (Nx) rat model of focal segmental glomerulosclerosis were investigated.
    Summary · context
    Sections of control glomeruli from normal baseline Nx tissue and nonsclerotic and sclerotic glomeruli from 12 wk after 5/6 Nx were isolated by laser capture microdissection.

    This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.

  2. 02AnimalEndogenous levelAnimal study (in vivo)Mechanism

    In rats with 5/6 nephrectomy, thymosin beta4 immunostaining was increased in sclerotic glomeruli, mainly in endothelial cells.

    In plain wordsIn rats with kidney damage, the body's own thymosin beta4 was higher in scarred kidney filters, mainly in endothelial cells.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseThymosin beta4 immunostaining in sclerotic glomeruli
    Study

    ratn: not reported in source

    5/6 nephrectomy model of focal segmental glomerulosclerosis
    Outcome group
    Kidney function · Kidney and urinary

    Source sentences

    Summary
    Thymosin beta4 immunostaining was increased in sclerotic glomeruli, predominantly in endothelial cells.
    2 context sentences
    Summary · context
    Protein expression profiles linked to sclerosis in the 5/6 nephrectomy (Nx) rat model of focal segmental glomerulosclerosis were investigated.
    Summary · context
    Sections of control glomeruli from normal baseline Nx tissue and nonsclerotic and sclerotic glomeruli from 12 wk after 5/6 Nx were isolated by laser capture microdissection.

    This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.

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).

  1. 03LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In cultured glomerular endothelial cells, RNAi downregulation of thymosin beta4 decreased angiotensin II-induced plasminogen activator inhibitor-1 expression.

    In plain wordsIn cells, lowering the cells' own thymosin beta4 with RNAi reduced the rise in PAI-1 caused by angiotensin II.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseAngiotensin II-induced PAI-1 expression after thymosin beta4 knockdown
    Study

    n: not reported in source

    cultured glomerular endothelial cells
    Outcome group
    Kidney function · Kidney and urinary

    Source sentences

    Summary
    Downregulation of thymosin beta4 by RNAi in cultured glomerular endothelial cells decreased angiotensin II-induced plasminogen activator inhibitor-1 expression.
    2 context sentences
    Summary · context
    Protein expression profiles linked to sclerosis in the 5/6 nephrectomy (Nx) rat model of focal segmental glomerulosclerosis were investigated.
    Summary · context
    Sections of control glomeruli from normal baseline Nx tissue and nonsclerotic and sclerotic glomeruli from 12 wk after 5/6 Nx were isolated by laser capture microdissection.

    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).

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

Terms as the source lists them.

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