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Study · In vitro (cells) · 2001

3 results

Defect in insulin-like growth factor-1 survival mechanism in atherosclerotic plaque-derived vascular smooth muscle cells is mediated by reduced surface binding and signaling.

Patel VA, Zhang QJ, Siddle K, Soos MA, Goddard M, Weissberg PL, Bennett MR

Circulation research1 May 2001Cited by 74 (Europe PMC)

PMID11348998 (opens in a new tab)DOI10.1161/hh0901.090305 (opens in a new tab)PepBankPUB-11348998
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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

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In human plaque-derived vascular smooth muscle cells, long R3 IGF-1 increased cell survival to the level of normal medial cells.

    In plain wordsIn lab-grown plaque cells from human arteries, an IGF-1 analogue raised cell survival to the level of normal artery wall cells.

    Peptide
    IGF-1 LR3
    Outcome
    IncreasepVSMC survival with long R3 IGF-1
    Study

    humann: not reported in source

    human plaque-derived vascular smooth muscle cells (pVSMCs)
    Outcome group
    Cell viability and death · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    pVSMCs expressed and secreted high levels of IGF-1 binding proteins (IGFBPs), and the IGF-1 analogues, long R3 and Des 1,3 IGF-1, which do not bind to IGFBPs, were able to increase pVSMC survival to normal medial VSMC levels
    1 context sentence
    Summary · context
    We have previously found that human plaque-derived VSMCs (pVSMCs) are intrinsically sensitive to apoptosis and not responsive to the protective effects of insulin-like growth factor-1 (IGF-1).
  2. 02LabIn vitro (cells)Mechanism

    In human plaque-derived vascular smooth muscle cells, the survival effect of long R3 IGF-1 was mediated by phosphatidylinositol 3-kinase.

    In plain wordsIn lab-grown plaque cells from human arteries, the survival effect of an IGF-1 analogue worked through the PI3K pathway.

    Peptide
    IGF-1 LR3
    Outcome
    Not applicablePI3K dependence of the long R3 survival effect
    Study

    humann: not reported in source

    human plaque-derived vascular smooth muscle cells (pVSMCs)
    Outcome group
    Cell viability and death · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The long R3 survival effect was phosphatidylinositol 3-kinase-mediated
    1 context sentence
    Summary · context
    We have previously found that human plaque-derived VSMCs (pVSMCs) are intrinsically sensitive to apoptosis and not responsive to the protective effects of insulin-like growth factor-1 (IGF-1).
  3. 03LabIn vitro (cells)Mechanism

    In human plaque-derived vascular smooth muscle cells, the survival effect of long R3 IGF-1 was not dependent on Akt activity alone.

    In plain wordsIn lab-grown plaque cells from human arteries, the survival effect of an IGF-1 analogue did not depend on Akt activity alone.

    Peptide
    IGF-1 LR3
    Outcome
    Not applicableAkt dependence of the long R3 survival effect
    Study

    humann: not reported in source

    human plaque-derived vascular smooth muscle cells (pVSMCs)
    Outcome group
    Cell viability and death · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    but it was not dependent on Akt activity alone.
    1 context sentence
    Summary · context
    We have previously found that human plaque-derived VSMCs (pVSMCs) are intrinsically sensitive to apoptosis and not responsive to the protective effects of insulin-like growth factor-1 (IGF-1).

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, 21:44 UTC

    Study results updated

  2. Version 1

    13 Oct 2026, 16:31 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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