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Study · In vitro (cells) · bovine · 2009

3 results

Mitochondria-derived reactive oxygen species mediate heme oxygenase-1 expression in sheared endothelial cells.

Han Z, Varadharaj S, Giedt RJ, Zweier JL, Szeto HH, Alevriadou BR

The Journal of pharmacology and experimental therapeutics8 Jan 2009Cited by 72 (Europe PMC)

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

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

  1. 01LabIn vitro (cells)Mechanism

    In bovine aortic endothelial cells under shear stress, SS‑31 markedly inhibited the increase in heme oxygenase-1 (HO-1) expression.

    In plain wordsIn cells, SS‑31 strongly blocked the rise in the protective protein HO-1 caused by flow-related stress.

    Outcome
    DecreaseShear-induced HO-1 protein expression
    Study

    bovinen: not reported in source

    Bovine aortic endothelial cells under shear stress
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The mitochondrial electron transport chain inhibitors, myxothiazol, rotenone, or antimycin A, and the mitochondria-targeted antioxidant peptide, Szeto-Schiller (SS)-31, which scavenges O(2)(*-), hydrogen peroxide (H(2)O(2)), peroxynitrite, and hydroxyl radicals, markedly inhibited the increase in HO-1 expression.
    1 context sentence
    Summary · context
    EC exposure to steady laminar shear stress causes a sustained increase in NO, a transient increase in reactive oxygen species (ROS), and activation of the HO-1 gene.
  2. 02LabIn vitro (cells)Mechanism

    In sheared bovine aortic endothelial cells, SS‑31 significantly inhibited the shear-induced MitoSOX fluorescence signal.

    In plain wordsIn cells, SS‑31 lowered the mitochondrial superoxide signal that rose under flow-related stress.

    Outcome
    DecreaseShear-induced mitochondrial superoxide (MitoSOX signal)
    Study

    bovinen: not reported in source

    Bovine aortic endothelial cells under shear stress
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 significantly inhibited both the shear-induced MitoSOX and DCF fluorescence signals.
    1 context sentence
    Summary · context
    EC exposure to steady laminar shear stress causes a sustained increase in NO, a transient increase in reactive oxygen species (ROS), and activation of the HO-1 gene.
  3. 03LabIn vitro (cells)Mechanism

    In sheared bovine aortic endothelial cells, SS‑31 significantly inhibited the shear-induced DCF fluorescence signal.

    In plain wordsIn cells, SS‑31 lowered the peroxide signal that rose under flow-related stress.

    Outcome
    DecreaseShear-induced intracellular peroxides (DCF signal)
    Study

    bovinen: not reported in source

    Bovine aortic endothelial cells under shear stress
    Outcome group
    Mitochondrial function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    SS-31 significantly inhibited both the shear-induced MitoSOX and DCF fluorescence signals.
    1 context sentence
    Summary · context
    EC exposure to steady laminar shear stress causes a sustained increase in NO, a transient increase in reactive oxygen species (ROS), and activation of the HO-1 gene.

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

    10 Oct 2026, 08:19 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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