Skip to content

Study · Not a test of the peptide alone · 2016

6 results

Increased nuclear stiffness via FAK-ERK1/2 signaling is necessary for synthetic mechano-growth factor E peptide-induced tenocyte migration.

Zhang B, Luo Q, Chen Z, Shi Y, Ju Y, Yang L, Song G

Scientific reports8 Jan 2016Cited by 22 (Europe PMC)

PMID26742689 (opens in a new tab)PMCIDPMC4705462 (opens in a new tab)DOI10.1038/srep18809 (opens in a new tab)PepBankPUB-26742689
Download PDFPubMedAsk about this study
Jump to 6 results

Summary

We have previously reported that a synthetic mechano-growth factor (MGF) C-terminal E-domain with 25 amino acids (MGF-C25E) promotes rat tenocyte migration through the FAK-ERK1/2 signaling pathway. However, the role of the nucleus in MGF-C25E-promoted tenocyte migration and the molecular mechanisms involved remain unclear. In this study, we demonstrate that MGF-C25E increases the Young's modulus of tenocytes through the FAK-ERK1/2 signaling pathway. This increase is not accompanied by an obvious change in the expression of Lamin A/C but is accompanied by significant chromatin condensation, indicating that MGF-C25E-induced chromatin condensation may contribute to the increased nuclear stiffness. Moreover, DNA methylation is observed in MGF-C25E-treated tenocytes. Inhibition of DNA methylation suppresses the elevation in chromatin condensation, in nuclear stiffness, and in tenocyte migration induced by MGF-C25E. The inhibition of the focal adhesion kinase (FAK) or extracellular signal regulated kinase 1/2 (ERK1/2) signals represses MGF-C25E-promoted DNA methylation. It also abolishes chromatin condensation, nuclear stiffness, and cell migration. Taken together, our results suggest that MGF-C25E promotes tenocyte migration by increasing nuclear stiffness via the FAK-ERK1/2 signaling pathway. This provides strong evidence for the role of nuclear mechanics in tenocyte migration and new insight into the molecular mechanisms of MGF-promoted tenocyte migration.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study6

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone6

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. 01LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism

    In rat tenocytes, the MGF fragment MGF-C25E increased the Young's modulus through the FAK-ERK1/2 signaling pathway.

    In plain wordsIn rat tendon cells in the lab, an MGF fragment made cells stiffer through a signaling pathway.

    Peptide
    MGF / PEG-MGF
    Outcome
    IncreaseTenocyte nuclear stiffness (Young's modulus)
    Study

    ratn: not reported in source

    rat tenocytes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    In this study, we demonstrate that MGF-C25E increases the Young's modulus of tenocytes through the FAK-ERK1/2 signaling pathway.
    1 context sentence
    Summary · context
    We have previously reported that a synthetic mechano-growth factor (MGF) C-terminal E-domain with 25 amino acids (MGF-C25E) promotes rat 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. 02LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism

    In rat tenocytes, MGF-C25E was accompanied by significant chromatin condensation.

    In plain wordsIn rat tendon cells in the lab, an MGF fragment was accompanied by tighter packing of DNA in the nucleus.

    Peptide
    MGF / PEG-MGF
    Outcome
    IncreaseChromatin condensation
    Study

    ratn: not reported in source

    rat tenocytes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    This increase is not accompanied by an obvious change in the expression of Lamin A/C but is accompanied by significant chromatin condensation, indicating that MGF-C25E-induced chromatin condensation may contribute to the increased nuclear stiffness.
    1 context sentence
    Summary · context
    We have previously reported that a synthetic mechano-growth factor (MGF) C-terminal E-domain with 25 amino acids (MGF-C25E) promotes rat 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.

  3. 03LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism

    In rat tenocytes, MGF-C25E caused no obvious change in the expression of Lamin A/C.

    In plain wordsIn rat tendon cells in the lab, an MGF fragment did not obviously change the nuclear protein Lamin A/C.

    Peptide
    MGF / PEG-MGF
    Outcome
    No significant changeLamin A/C expression
    Study

    ratn: not reported in source

    rat tenocytes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    This increase is not accompanied by an obvious change in the expression of Lamin A/C but is accompanied by significant chromatin condensation, indicating that MGF-C25E-induced chromatin condensation may contribute to the increased nuclear stiffness.
    1 context sentence
    Summary · context
    We have previously reported that a synthetic mechano-growth factor (MGF) C-terminal E-domain with 25 amino acids (MGF-C25E) promotes rat 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.

  4. 04LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism

    DNA methylation was observed in rat tenocytes treated with MGF-C25E.

    In plain wordsIn rat tendon cells in the lab, an MGF fragment was followed by DNA methylation.

    Peptide
    MGF / PEG-MGF
    Outcome
    IncreaseDNA methylation
    Study

    ratn: not reported in source

    rat tenocytes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    Moreover, DNA methylation is observed in MGF-C25E-treated tenocytes.
    1 context sentence
    Summary · context
    We have previously reported that a synthetic mechano-growth factor (MGF) C-terminal E-domain with 25 amino acids (MGF-C25E) promotes rat 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.

  5. 05LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism

    In rat tenocytes, inhibition of DNA methylation suppressed the increases in chromatin condensation, nuclear stiffness and cell migration induced by MGF-C25E.

    In plain wordsIn rat tendon cells in the lab, blocking DNA methylation reduced the effects of an MGF fragment on nuclear stiffness and cell movement.

    Peptide
    MGF / PEG-MGF
    Outcome
    DecreaseEffect of DNA methylation inhibition on MGF-C25E-induced chromatin condensation, nuclear stiffness and migration
    Study

    ratn: not reported in source

    rat tenocytes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    Inhibition of DNA methylation suppresses the elevation in chromatin condensation, in nuclear stiffness, and in tenocyte migration induced by MGF-C25E.

    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.

  6. 06LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism

    In rat tenocytes, inhibition of FAK or ERK1/2 signals repressed MGF-C25E-promoted DNA methylation and abolished chromatin condensation, nuclear stiffness and cell migration.

    In plain wordsIn rat tendon cells in the lab, blocking two signaling proteins stopped an MGF fragment's effects on DNA methylation, nuclear stiffness and cell movement.

    Peptide
    MGF / PEG-MGF
    Outcome
    DecreaseEffect of FAK or ERK1/2 inhibition on MGF-C25E-promoted DNA methylation, chromatin condensation, nuclear stiffness and migration
    Study

    ratn: not reported in source

    rat tenocytes
    Outcome group
    Receptor activity and mechanism · Musculoskeletal

    Source sentences

    Summary
    The inhibition of the focal adhesion kinase (FAK) or extracellular signal regulated kinase 1/2 (ERK1/2) signals represses MGF-C25E-promoted DNA methylation. It also abolishes chromatin condensation, nuclear stiffness, and cell migration.

    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.

PepBank is a research reference. Talk to a doctor before you use any peptide.