ArticlePloS one2014
T-plastin expression downstream to the calcineurin/NFAT pathway is involved in keratinocyte migration.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Application of Bioactive Natural Compounds to Promote Cell Proliferation and Migration in the Wound Healing Process.Results and problems in cell differentiation · 2026Review
- Human Plastins are Novel Cytoskeletal pH Sensors with a Reduced F-actin Bundling Capacity at Basic pH.Journal of molecular biology · 2025Article
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- Coencapsulation of Immunosuppressive Drug with Anti-Inflammatory Molecule in Pickering Emulsions as an Innovative Therapeutic Approach for Inflammatory Dermatoses.JID innovations : skin science from molecules to population health · 2024Article
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- The intricate mechanism of PLS3 in bone homeostasis and disease.Frontiers in endocrinology · 2023Review
- The actin-bundling protein, PLS3, is part of the mechanoresponsive machinery that regulates osteoblast mineralization.Frontiers in cell and developmental biology · 2023Article
- Calcineurin-nuclear factor for activated T cells (NFAT) signaling in pathophysiology of wound healing.Inflammation and regeneration · 2021Review
- Plastin 3 in health and disease: a matter of balance.Cellular and molecular life sciences : CMLS · 2021Review
- Osteogenesis imperfecta mutations in plastin 3 lead to impaired calcium regulation of actin bundling.Bone research · 2020Article
- Activation of Parathyroid Hormone 2 Receptor Induces Decorin Expression and Promotes Wound Repair.The Journal of investigative dermatology · 2017Article
- The role of Orai-STIM calcium channels in melanocytes and melanoma.The Journal of physiology · 2016Review
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cutaneous wound healing requires keratinocyte proliferation, migration and differentiation to restore the barrier function of the skin. The calcineurin/nuclear factor of activated-T-cell (NFAT) signaling pathway has been recently shown to be involved in keratinocyte growth, differentiation and migration. It is induced by an increased intracellular calcium rate and its inhibition results in decreased capacities of keratinocytes to migrate. Nevertheless, the link between calcineurin activation and keratinocyte migration remains unknown. Recently, Orai1, a pore subunit of a store-operated calcium channel that favors calcium influx, was shown to play a critical role to control proliferation and migration of basal keratinocytes. Of interest, the actin-bundling T-plastin is crucial in cell motility through cross-linking to actin filament and its synthesis was shown to be induced by calcium influx and regulated by the calcineurin/NFAT pathway in tumor Sezary cells. We investigated herein the role of the calcineurin/NFAT pathway-dependent T-plastin in keratinocyte migration, by quantifying T-plastin expression in keratinocytes and by analyzing their migration under calcineurin inhibition or knockdown of NFAT2 or T-plastin. We did confirm the role of the calcineurin/NFAT pathway in keratinocyte migration as shown by their decreased capacities to migrate after FK506 treatment or siNFAT2 transfection in both scratching and Boyden assays. The expression of NFAT2 and T-plastin in keratinocytes was decreased under FK506 treatment, suggesting that T-plastin plays a role in keratinocyte migration downstream to the calcineurin/NFAT pathway. Accordingly, siRNA knockdown of T-plastin expression also decreased their migration capacities. Actin lamellipodia formation as well as FAK and β6-integrin expression were also significantly decreased after treatment with FK506 or siRNA, reinforcing that NFAT2-dependent T-plastin expression plays a role in keratinocyte migration. These results indicate that T-plastin might be considered as a major actor in the mechanisms underlying calcineurin/NFAT-dependent keratinocyte migration and may explain wound-healing defects observed in patients under calcineurin inhibitor long-term treatment.
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