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Study · In vitro (cells) · 1999

7 results

Insulin-like growth factor (IGF)-I regulates IGF-binding protein-5 gene expression through the phosphatidylinositol 3-kinase, protein kinase B/Akt, and p70 S6 kinase signaling pathway.

Duan C, Liimatta MB, Bottum OL

The Journal of biological chemistry1 Dec 1999Cited by 62 (Europe PMC)

PMID10601276 (opens in a new tab)DOI10.1074/jbc.274.52.37147 (opens in a new tab)PepBankPUB-10601276
Publisher pagePubMedAsk about this study
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Summary

Expression of the insulin-like growth factor-binding protein 5 (IGFBP-5) gene in vascular smooth muscle cells is up-regulated by IGF-I through an IGF-I receptor-mediated mechanism. In this study, we studied the possible involvement of the mitogen-activated protein kinase (MAPK) and PI 3-kinase signaling pathways in mediating IGF-I-regulated IGFBP-5 gene expression. The addition of Des(1-3)IGF-I, an IGF analog with reduced affinity to IGFBPs, resulted in a transient activation of p44 and p42 MAPK. Inhibition of the MAPK activation by PD98059, however, did not affect IGF-I-stimulated IGFBP-5 expression. Des(1-3)IGF-I treatment also strongly activated PI 3-kinase. This activation was probably mediated through IRS-1, because IGF-I stimulation resulted in a significant increase in IRS-1- but not IRS-2-associated PI 3-kinase activity. This activation occurred within 5 min and was sustained at high levels for over 6 h. Likewise, Des(1-3)IGF-I caused a long lasting activation of PKB/Akt and p70(s6k). When LY294002 and wortmannin, two specific inhibitors of PI 3-kinase, were added with Des(1-3)IGF-I, the IGF-I-regulated IGFBP-5 expression was negated. The addition of rapamycin, which inhibits IGF-I-induced p70(s6k) activation, significantly inhibited IGF-I-regulated IGFBP-5 gene expression. These results suggest that the action of IGF-I on IGFBP-5 gene expression requires the activation of the PI 3-kinase-PKB/Akt-p70(s6k) pathway but not the MAPK pathway in vascular smooth muscle cells.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study7

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

  1. 01LabIn vitro (cells)Mechanism

    In vascular smooth muscle cells, Des(1‑3)IGF-I transiently activated p44 MAPK.

    In plain wordsIn cells, Des(1‑3)IGF-I transiently activated p44 MAPK.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    Increasep44 MAPK activation
    Study

    n: not reported in source

    Vascular smooth muscle cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The addition of Des(1-3)IGF-I, an IGF analog with reduced affinity to IGFBPs, resulted in a transient activation of p44 and p42 MAPK.
    1 context sentence
    Summary · context
    In this study, we studied the possible involvement of the mitogen-activated protein kinase (MAPK) and PI 3-kinase signaling pathways in mediating IGF-I-regulated IGFBP-5 gene expression.
  2. 02LabIn vitro (cells)Mechanism

    In vascular smooth muscle cells, Des(1‑3)IGF-I transiently activated p42 MAPK.

    In plain wordsIn cells, Des(1‑3)IGF-I transiently activated p42 MAPK.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    Increasep42 MAPK activation
    Study

    n: not reported in source

    Vascular smooth muscle cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The addition of Des(1-3)IGF-I, an IGF analog with reduced affinity to IGFBPs, resulted in a transient activation of p44 and p42 MAPK.
    1 context sentence
    Summary · context
    In this study, we studied the possible involvement of the mitogen-activated protein kinase (MAPK) and PI 3-kinase signaling pathways in mediating IGF-I-regulated IGFBP-5 gene expression.
  3. 03LabIn vitro (cells)Mechanism

    In vascular smooth muscle cells, Des(1‑3)IGF-I strongly activated PI 3-kinase.

    In plain wordsIn cells, Des(1‑3)IGF-I strongly activated PI 3-kinase.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    IncreasePI 3-kinase activation
    Study

    n: not reported in source

    Vascular smooth muscle cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Des(1-3)IGF-I treatment also strongly activated PI 3-kinase.
    2 context sentences
    Summary · context
    This activation occurred within 5 min and was sustained at high levels for over 6 h.
    Summary · context
    In this study, we studied the possible involvement of the mitogen-activated protein kinase (MAPK) and PI 3-kinase signaling pathways in mediating IGF-I-regulated IGFBP-5 gene expression.
  4. 04LabIn vitro (cells)Mechanism

    In vascular smooth muscle cells, Des(1‑3)IGF-I caused sustained PKB/Akt activation.

    In plain wordsIn cells, Des(1‑3)IGF-I caused sustained PKB/Akt activation.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    IncreasePKB/Akt activation
    Study

    n: not reported in source

    Vascular smooth muscle cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Likewise, Des(1-3)IGF-I caused a long lasting activation of PKB/Akt and p70(s6k).
    1 context sentence
    Summary · context
    In this study, we studied the possible involvement of the mitogen-activated protein kinase (MAPK) and PI 3-kinase signaling pathways in mediating IGF-I-regulated IGFBP-5 gene expression.
  5. 05LabIn vitro (cells)Mechanism

    In vascular smooth muscle cells, Des(1‑3)IGF-I caused sustained p70 S6 kinase activation.

    In plain wordsIn cells, Des(1‑3)IGF-I caused sustained p70 S6 kinase activation.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    Increasep70 S6 kinase activation
    Study

    n: not reported in source

    Vascular smooth muscle cells
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Likewise, Des(1-3)IGF-I caused a long lasting activation of PKB/Akt and p70(s6k).
    1 context sentence
    Summary · context
    In this study, we studied the possible involvement of the mitogen-activated protein kinase (MAPK) and PI 3-kinase signaling pathways in mediating IGF-I-regulated IGFBP-5 gene expression.

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. 06LabNot a test of IGF-1 DES (des(1-3)IGF-I) aloneIn vitro (cells)Mechanism

    In vascular smooth muscle cells, LY294002 negated Des(1‑3)IGF-I-regulated IGFBP-5 expression.

    In plain wordsIn cells, adding LY294002 blocked Des(1‑3)IGF-I-regulated IGFBP-5 expression compared with Des(1‑3)IGF-I alone.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    DecreaseIGFBP-5 expression with LY294002
    Study

    n: not reported in source

    Vascular smooth muscle cells
    Comparator
    Des(1-3)IGF-I without LY294002
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    When LY294002 and wortmannin, two specific inhibitors of PI 3-kinase, were added with Des(1-3)IGF-I, the IGF-I-regulated IGFBP-5 expression was negated.
    1 context sentence
    Summary · context
    In this study, we studied the possible involvement of the mitogen-activated protein kinase (MAPK) and PI 3-kinase signaling pathways in mediating IGF-I-regulated IGFBP-5 gene expression.

    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. 07LabNot a test of IGF-1 DES (des(1-3)IGF-I) aloneIn vitro (cells)Mechanism

    In vascular smooth muscle cells, wortmannin negated Des(1‑3)IGF-I-regulated IGFBP-5 expression.

    In plain wordsIn cells, adding wortmannin blocked Des(1‑3)IGF-I-regulated IGFBP-5 expression compared with Des(1‑3)IGF-I alone.

    Peptide
    IGF-1 DES (des(1-3)IGF-I)
    Outcome
    DecreaseIGFBP-5 expression with wortmannin
    Study

    n: not reported in source

    Vascular smooth muscle cells
    Comparator
    Des(1-3)IGF-I without wortmannin
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    When LY294002 and wortmannin, two specific inhibitors of PI 3-kinase, were added with Des(1-3)IGF-I, the IGF-I-regulated IGFBP-5 expression was negated.
    1 context sentence
    Summary · context
    In this study, we studied the possible involvement of the mitogen-activated protein kinase (MAPK) and PI 3-kinase signaling pathways in mediating IGF-I-regulated IGFBP-5 gene expression.

    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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