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Study · Animal study (in vivo) · rabbit · 2019

7 results

MGF E peptide improves anterior cruciate ligament repair by inhibiting hypoxia-induced cell apoptosis and accelerating angiogenesis.

Sha Y, Yang L, Lv Y

Journal of cellular physiology14 Oct 2018Cited by 15 (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 study7

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In a rabbit ACL rupture model, MGF E peptide decreased HIF-1α expression.

    In plain wordsIn rabbits with a torn ACL, MGF E peptide lowered HIF-1α, a protein that responds to low oxygen.

    Outcome
    DecreaseHIF-1α expression after ACL rupture
    Study

    rabbitn: not reported in source

    ACL rupture model
    Outcome group
    Tendon and ligament healing · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In rabbit ACL rupture model, MGF E peptide also decreased HIF-1α expression levels, cell apoptosis, and facilitated cell proliferation.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In a rabbit ACL rupture model, MGF E peptide decreased cell apoptosis.

    In plain wordsIn rabbits with a torn ACL, MGF E peptide reduced cell death in the injured ligament.

    Outcome
    DecreaseCell apoptosis after ACL rupture
    Study

    rabbitn: not reported in source

    ACL rupture model
    Outcome group
    Tendon and ligament healing · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In rabbit ACL rupture model, MGF E peptide also decreased HIF-1α expression levels, cell apoptosis, and facilitated cell proliferation.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In a rabbit ACL rupture model, MGF E peptide facilitated cell proliferation.

    In plain wordsIn rabbits with a torn ACL, MGF E peptide increased cell growth in the injured ligament.

    Outcome
    IncreaseCell proliferation after ACL rupture
    Study

    rabbitn: not reported in source

    ACL rupture model
    Outcome group
    Tendon and ligament healing · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In rabbit ACL rupture model, MGF E peptide also decreased HIF-1α expression levels, cell apoptosis, and facilitated cell proliferation.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    After ACL injury, MGF could accelerate angiogenesis, probably through recruitment of proangiogenic cells via the SDF-1α/CXCR4 axis and stimulation of VEGFα expression.

    In plain wordsIn rabbits with a torn ACL, MGF may have sped up the growth of new blood vessels in the injury.

    Outcome
    IncreaseAngiogenesis after ACL injury
    Study

    rabbitn: not reported in source

    ACL rupture model
    Outcome group
    Tendon and ligament healing · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, MGF could accelerate angiogenesis after ACL injury probably owing to its recruitment of proangiogenesis cells by stromal cell-derived factor 1α/CXCR4 axis and stimulation of vascular endothelial growth factor α expression level.
    1 context sentence
    Summary · context
    In rabbit ACL rupture model, MGF E peptide also decreased HIF-1α expression levels, cell apoptosis, and facilitated cell proliferation.
  5. 05LabIn vitro (cells)Efficacy outcome

    In ACL fibroblasts under severe hypoxia, MGF E peptide protected the cells against apoptosis.

    In plain wordsIn lab-grown ligament cells short of oxygen, MGF E peptide protected the cells from dying.

    Outcome
    DecreaseHypoxia-induced apoptosis of ACL fibroblasts
    Study

    n: not reported in source

    ACL fibroblasts under severe hypoxia
    Comparator
    Hypoxia without MGF E peptide
    Outcome group
    Cell viability and death · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Fortunately, MGF E peptide effectively protected ACL fibroblasts against hypoxia-induced apoptosis through regulating caspase 3/7/9 mRNA, cleaved caspase 3 and apoptosis-relevant proteins expression levels.
    1 context sentence
    Summary · context
    In the current study, we explored the effects of mechanogrowth factor (MGF) E peptide on the hypoxia-induced apoptosis of ACL fibroblasts and relevant mechanisms.
  6. 06LabIn vitro (cells)Mechanism

    In ACL fibroblasts under severe hypoxia, MGF E peptide regulated caspase 3/7/9 mRNA, cleaved caspase 3 and apoptosis-related protein levels.

    In plain wordsIn lab-grown ligament cells short of oxygen, MGF E peptide changed the levels of several cell-death proteins.

    Outcome
    MixedCaspase 3/7/9 mRNA and apoptosis-related protein levels
    Study

    n: not reported in source

    ACL fibroblasts under severe hypoxia
    Outcome group
    Cell viability and death · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Fortunately, MGF E peptide effectively protected ACL fibroblasts against hypoxia-induced apoptosis through regulating caspase 3/7/9 mRNA, cleaved caspase 3 and apoptosis-relevant proteins expression levels.
    1 context sentence
    Summary · context
    In the current study, we explored the effects of mechanogrowth factor (MGF) E peptide on the hypoxia-induced apoptosis of ACL fibroblasts and relevant mechanisms.
  7. 07LabIn vitro (cells)Mechanism

    In ACL fibroblasts under severe hypoxia, the mitochondrial, MEK-ERK1/2 and PI3K-Akt pathways were involved in the effect of MGF E peptide on apoptosis.

    In plain wordsIn lab-grown ligament cells short of oxygen, three cell signalling pathways took part in how MGF E peptide acted on cell death.

    Outcome
    Not applicableSignalling pathways in hypoxia-induced apoptosis
    Study

    n: not reported in source

    ACL fibroblasts under severe hypoxia
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Simultaneously, mitochondrial, @@@MEK-ERK1/2 (extracellular-signal-regulated kinase 1/2), and phosphoinositide-3-kinase-protein kinase B (PI3K-Akt) pathways were involved in MGF E peptide regulating hypoxia-induced apoptosis of ACL fibroblasts.
    1 context sentence
    Summary · context
    In the current study, we explored the effects of mechanogrowth factor (MGF) E peptide on the hypoxia-induced apoptosis of ACL fibroblasts and relevant mechanisms.

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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