ArticleScientific reports2016
Increased nuclear stiffness via FAK-ERK1/2 signaling is necessary for synthetic mechano-growth factor E peptide-induced tenocyte migration.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 26 citations in OpenAlex.
- Mesenchymal stem cells: An efficient cell therapy for tendon repair (Review).International journal of molecular medicine · 2023Review
- Histone methyltransferase SUV39H1 regulates the Golgi complex via the nuclear envelope-spanning LINC complex.PloS one · 2023Article
- Effect of Mechanical Loading of Senescent Myoblasts on Their Myogenic Lineage Progression and Survival.Cells · 2022Article
- Confined migration induces heterochromatin formation and alters chromatin accessibility.iScience · 2022Article
- Why Use Adipose-Derived Mesenchymal Stem Cells in Tendinopathic Patients: A Systematic Review.Pharmaceutics · 2022Review
- Surface modification of electrospun fibers with mechano-growth factor for mitigating the foreign-body reaction.Bioactive materials · 2021Article
- Stretch-Induced Tenomodulin Expression Promotes Tenocyte Migration via F-Actin and Chromatin Remodeling.International journal of molecular sciences · 2021Article
- The Emerging Roles of Heterochromatin in Cell Migration.Frontiers in cell and developmental biology · 2020Review
- Article
- TGF-β1 Pretreatment Improves the Function of Mesenchymal Stem Cells in the Wound Bed.Frontiers in cell and developmental biology · 2017Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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