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Study · In vitro (cells) · rat · 2014

9 results

A synthetic mechano-growth factor E peptide promotes rat tenocyte migration by lessening cell stiffness and increasing F-actin formation via the FAK-ERK1/2 signaling pathway.

Zhang B, Luo Q, Mao X, Xu B, Yang L, Ju Y, Song G

Experimental cell research13 Jan 2014Cited by 27 (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 study9

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

  1. 01LabIn vitro (cells)Activity measurement

    In a scratch wound assay with rat tenocytes, MGF-C25E promoted cell migration.

    In plain wordsIn rat tendon cells in a lab dish, a synthetic MGF peptide made the cells move into a scratch faster.

    Outcome
    IncreaseTenocyte migration
    Study

    ratn: not reported in source

    rat tenocytes
    Outcome group
    Tendon and ligament healing · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We used a scratch wound assay in this study to demonstrate that MGF-C25E (a synthetic mechano-growth factor E peptide) promotes the migration of rat tenocytes
  2. 02LabIn vitro (cells)Mechanism

    In rat tenocytes, MGF-C25E was accompanied by higher expression of focal adhesion kinase (FAK).

    In plain wordsIn rat tendon cells in a lab dish, a synthetic MGF peptide was linked to more of the signal protein FAK.

    Outcome
    IncreaseFAK expression
    Study

    ratn: not reported in source

    rat tenocytes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    an elevation in the expression of the following signaling molecules: focal adhesion kinase (FAK)
  3. 03LabIn vitro (cells)Mechanism

    In rat tenocytes, MGF-C25E was accompanied by higher expression of ERK1/2.

    In plain wordsIn rat tendon cells in a lab dish, a synthetic MGF peptide was linked to more of the signal protein ERK1/2.

    Outcome
    IncreaseERK1/2 expression
    Study

    ratn: not reported in source

    rat tenocytes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    an elevation in the expression of the following signaling molecules: focal adhesion kinase (FAK) and extracellular signal regulated kinase1/2 (ERK1/2)
  4. 04LabIn vitro (cells)Mechanism

    In rat tenocytes, MGF-C25E treatment decreased cell stiffness measured as Young's modulus.

    In plain wordsIn rat tendon cells in a lab dish, a synthetic MGF peptide made the cells softer.

    Outcome
    DecreaseTenocyte Young's modulus (cell stiffness)
    Study

    ratn: not reported in source

    rat tenocytes
    Outcome group
    Tendon and ligament healing · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    modulus of tenocytes was decreased through treatment of MGF-C25E, and an obvious formation of pseudopodia and F-actin was observed in MGF-C25E-treated tenocytes.
  5. 05LabIn vitro (cells)Mechanism

    In rat tenocytes, MGF-C25E treatment increased the formation of pseudopodia.

    In plain wordsIn rat tendon cells in a lab dish, a synthetic MGF peptide caused more cell protrusions to form.

    Outcome
    IncreasePseudopodia formation
    Study

    ratn: not reported in source

    rat tenocytes
    Outcome group
    Tendon and ligament healing · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    an obvious formation of pseudopodia and F-actin was observed in MGF-C25E-treated tenocytes.
  6. 06LabIn vitro (cells)Mechanism

    In rat tenocytes, MGF-C25E treatment increased the formation of F-actin.

    In plain wordsIn rat tendon cells in a lab dish, a synthetic MGF peptide caused more F-actin to form.

    Outcome
    IncreaseF-actin formation
    Study

    ratn: not reported in source

    rat tenocytes
    Outcome group
    Tendon and ligament healing · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    an obvious formation of pseudopodia and F-actin was observed in MGF-C25E-treated tenocytes.

Studies that did not test the peptide alone3

In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.

  1. 07LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism

    In rat tenocytes, FAK and ERK1/2 pathway inhibitors blocked the migration induced by MGF-C25E.

    In plain wordsIn rat tendon cells in a lab dish, blocking FAK or ERK1/2 stopped the extra movement caused by a synthetic MGF peptide.

    Outcome
    DecreaseMigration after FAK or ERK1/2 inhibition
    Study

    ratn: not reported in source

    rat tenocytes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    Inhibitors of the FAK and ERK1/2 pathways inhibited the MGF-C25E-induced tenocyte migration, indicating that MGF-C25E promotes tenocyte migration through the FAK-ERK1/2 signaling pathway.

    In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.

  2. 08LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism

    In rat tenocytes, inhibiting FAK or ERK1/2 restored the decrease in Young's modulus caused by MGF-C25E.

    In plain wordsIn rat tendon cells in a lab dish, blocking FAK or ERK1/2 undid the softening caused by a synthetic MGF peptide.

    Outcome
    IncreaseYoung's modulus after FAK or ERK1/2 inhibition
    Study

    ratn: not reported in source

    rat tenocytes
    Outcome group
    Tendon and ligament healing · Musculoskeletal

    Source sentences

    Summary
    The inhibition of the FAK or ERK1/2 signals restored the decrease in Young's modulus and inhibited the formation of pseudopodia and F-actin.

    In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.

  3. 09LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism

    In rat tenocytes, inhibiting FAK or ERK1/2 reduced the formation of pseudopodia and F-actin seen with MGF-C25E.

    In plain wordsIn rat tendon cells in a lab dish, blocking FAK or ERK1/2 reduced the protrusions and F-actin caused by a synthetic MGF peptide.

    Outcome
    DecreasePseudopodia and F-actin after FAK or ERK1/2 inhibition
    Study

    ratn: not reported in source

    rat tenocytes
    Outcome group
    Tendon and ligament healing · Musculoskeletal

    Source sentences

    Summary
    The inhibition of the FAK or ERK1/2 signals restored the decrease in Young's modulus and inhibited the formation of pseudopodia and F-actin.

    In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.

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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