ArticleBritish journal of pharmacology2018
Modulation of sonic hedgehog-induced mouse embryonic stem cell behaviours through E-cadherin expression and integrin β1-dependent F-actin formation.
Article in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Decoding Rho GTPase signalling networks in directed cell migration.Frontiers in cell and developmental biology · 2026Review
- Hedgehog Signaling Functions in Spermatogenesis and Keeping Hemolymph-Testis Barrier Stability inInternational journal of molecular sciences · 2025Article
- Extracellular matrix gene set and microRNA network in intestinal ischemia-reperfusion injury: Insights from RNA sequencing for diagnosis and therapy.World journal of gastrointestinal surgery · 2025Review
- Review
- Differential Therapeutic Effect of Extracellular Vesicles Derived by Bone Marrow and Adipose Mesenchymal Stem Cells on Wound Healing of Diabetic Ulcers and Correlation to Their Cargoes.International journal of molecular sciences · 2021Article
- Intertwined Signaling Pathways Governing Tooth Development: A Give-and-Take Between Canonical Wnt and Shh.Frontiers in cell and developmental biology · 2021Review
- Metformin upregulates the expression of Gli1 in vascular endothelial cells in hyperoxia-exposed neonatal mice.American journal of translational research · 2020Article
- Modulation of sonic hedgehog-induced mouse embryonic stem cell behaviours through E-cadherin expression and integrin β1-dependent F-actin formation.British journal of pharmacology · 2018Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeThe sonic hedgehog pathway (Shh) plays a central role in maintaining stem cell function and behaviour in various processes related to self-renewal and tissue regeneration. However, the therapeutic effect of Shh on mouse embryonic stem cells (mESCs) has not yet been clearly elucidated. Thus, we investigated the effect of Shh on the regulation of mESC behaviour as well as the effect of Shh-pretreated mESCs in skin wound healing. EXPERIMENTAL APPROACH: The underlying mechanisms of Shh signalling pathway in growth and motility of mESCs were investigated using Western blot analysis, a cell proliferation assay and cell migration assay. In addition, the effect of Shh-pretreated mESCs in skin wound healing was determined using a mouse excisional wound splinting model. KEY
resultsShh disrupted the adherens junction through proteolysis by activating MMPs. In addition, the release of β-catenin from adherens junctions mediated by Shh led to cell cycle-dependent mESC proliferation. Shh-mediated Gli1 expression led to integrin β1 up-regulation, followed by FAK and Src phosphorylation. Furthermore, among the Rho-GTPases, Rac1 and Cdc42 were activated in a Shh-dependent manner while F-actin expression was suppressed by Rac1 and Cdc42 siRNA transfection. Consistent with the in vitro results, the skin wound healing assay revealed that Shh-treated mESCs increased angiogenesis and skin wound repair compared to that in Shh-treated mESCs transfected with integrin β1 siRNA in vivo. CONCLUSIONS AND IMPLICATIONS: Our results imply that Shh induces adherens junction disruption and integrin β1-dependent F-actin formation by a mechanism involving FAK/Src and Rac1/Cdc42 signalling pathways in mESCs.
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