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Study · In vitro (cells) · mouse · 1996

3 results

Insulin-like growth factor-II is an autocrine survival factor for differentiating myoblasts.

Stewart CE, Rotwein P

The Journal of biological chemistry1 May 1996Cited by 148 (Europe PMC)

PMID8626686 (opens in a new tab)DOI10.1074/jbc.271.19.11330 (opens in a new tab)PepBankPUB-08626686
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Summary

Recent studies indicate that insulin-like growth factor-II (IGF-II) acts as an autocrine differentiation factor for skeletal myoblasts in culture. IGF-II mRNA and protein are induced as early events in muscle differentiation, and the rate and extent of IGF-II secretion correlate with both biochemical and morphological differentiation. Here we show that IGF-II also functions as an essential survival factor during the transition from proliferating to differentiating myoblasts. Stably transfected C2 muscle cell lines were established in which a mouse IGF-II cDNA was expressed in the antisense orientation relative to the constitutively active Moloney sarcoma virus promoter. IGF-II antisense cells proliferated normally in growth medium containing 20% serum but underwent rapid death when placed in low serum differentiation medium. Death was accompanied by characteristic markers of apoptosis with more than 90% of cells showing DNA fragmentation within 12-16 h. Myoblast death was prevented by IGF-I, des [1-3] IGF-I, IGF-II, and insulin with a dose potency consistent with activation of the IGF-I receptor; death also could be blocked by the protein synthesis inhibitor, cycloheximide. Exogenous IGFs additionally stimulated passage through a single cell cycle and subsequently induced terminal differentiation. Cell survival and cell cycle progression also were enhanced by fibroblast growth factor-2 and platelet-derived growth factor-bb, but these peptides did not promote differentiation. Our results define a novel system for studying apoptotic cell death and its prevention by growth factors, underscore the importance of IGF action in minimizing inappropriate cell death, and indicate that shared signal transduction pathways may mediate myoblast survival in vitro.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In IGF-II antisense myoblasts, des [1-3] IGF-I prevented death in low-serum differentiation medium.

    In plain wordsIn cells, des [1-3] IGF-I prevented myoblast death in low-serum medium.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    DecreaseMyoblast death
    Study

    mousen: not reported in source

    IGF-II antisense C2 myoblasts
    Outcome group
    Muscle injury and repair · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Myoblast death was prevented by IGF-I, des [1-3] IGF-I, IGF-II, and insulin with a dose potency consistent with activation of the IGF-I receptor
    2 context sentences
    Summary · context
    IGF-II antisense cells proliferated normally in growth medium containing 20% serum but underwent rapid death when placed in low serum differentiation medium.
    Summary · context
    Stably transfected C2 muscle cell lines were established in which a mouse IGF-II cDNA was expressed in the antisense orientation relative to the constitutively active Moloney sarcoma virus promoter.

Studies that did not test the peptide alone2

In this study, IGF-1 DES (des(1-3)IGF-I) 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 IGF-1 DES (des(1-3)IGF-I).

  1. 02LabNot a test of IGF-1 DES (des(1-3)IGF-I) aloneIn vitro (cells)Activity measurement

    In IGF-II antisense myoblasts, exogenous IGFs as a group stimulated passage through a single cell cycle.

    In plain wordsIn cells, exogenous IGFs as a group stimulated passage through one cell cycle.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    IncreaseCell cycle passage
    Study

    mousen: not reported in source

    IGF-II antisense C2 myoblasts
    Outcome group
    Muscle injury and repair · Musculoskeletal

    Source sentences

    Summary
    Exogenous IGFs additionally stimulated passage through a single cell cycle and subsequently induced terminal differentiation.
    1 context sentence
    Summary · context
    Stably transfected C2 muscle cell lines were established in which a mouse IGF-II cDNA was expressed in the antisense orientation relative to the constitutively active Moloney sarcoma virus promoter.

    In this study, IGF-1 DES (des(1-3)IGF-I) 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 IGF-1 DES (des(1-3)IGF-I).

  2. 03LabNot a test of IGF-1 DES (des(1-3)IGF-I) aloneIn vitro (cells)Efficacy outcome

    In IGF-II antisense myoblasts, exogenous IGFs as a group induced terminal differentiation.

    In plain wordsIn cells, exogenous IGFs as a group induced terminal muscle differentiation.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    IncreaseTerminal differentiation
    Study

    mousen: not reported in source

    IGF-II antisense C2 myoblasts
    Outcome group
    Muscle injury and repair · Musculoskeletal

    Source sentences

    Summary
    Exogenous IGFs additionally stimulated passage through a single cell cycle and subsequently induced terminal differentiation.
    1 context sentence
    Summary · context
    Stably transfected C2 muscle cell lines were established in which a mouse IGF-II cDNA was expressed in the antisense orientation relative to the constitutively active Moloney sarcoma virus promoter.

    In this study, IGF-1 DES (des(1-3)IGF-I) 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 IGF-1 DES (des(1-3)IGF-I).

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 3Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 2

    21 Oct 2026, 13:52 UTC

    Study data updated · source update from Europe PMC

  3. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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