ArticleBMC immunology2017
Poly I:C induces collective migration of HaCaT keratinocytes via IL-8.
Article in BMC immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 46 citations in OpenAlex.
- A Novel Multi-Component Formulation Reduces Inflammation In Vitro and Clinically Lessens the Symptoms of Chronic Eczematous Skin.International journal of molecular sciences · 2023Trial
- The therapeutic potential of transposable element activity modulation.EMBO molecular medicine · 2026Review
- From traditional remedy toFrontiers in pharmacology · 2026Article
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- TLR3 activation mediates partial epithelial-to-mesenchymal transition in human keratinocytes.Life science alliance · 2024Article
- Molecular mechanisms of thalidomide effectiveness on COVID-19 patients explained: ACE2 is a new ΔNp63α target gene.Journal of molecular medicine (Berlin, Germany) · 2024Article
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- IL-8 (CXCL8) Correlations with Psychoneuroimmunological Processes and Neuropsychiatric Conditions.Journal of personalized medicine · 2024Review
- Keratin isoform shifts modulate motility signals during wound healing.bioRxiv : the preprint server for biology · 2024Article
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- Exploring the Functions of Mutant p53 throughCurrent issues in molecular biology · 2024Article
- Inflammatory Response AgainstFrontiers in immunology · 2022Article
- Type-2 epithelial-mesenchymal transition in oral mucosal nonneoplastic diseases.Frontiers in immunology · 2022Review
- NaHCOAnnals of dermatology · 2021Article
- Therapeutic candidates for keloid scars identified by qualitative review of scratch assay research for wound healing.PloS one · 2021Review
- Protective Effects ofInternational journal of medical sciences · 2021Article
- Anti-Acne Vulgaris Effects of Pedunculagin from the Leaves ofMolecules (Basel, Switzerland) · 2020Article
- Enhanced Wound Healing- and Inflammasome-Associated Gene Expression in TNFAIP3-Interacting Protein 1- (TNIP1-) Deficient HaCaT Keratinocytes Parallels Reduced Reepithelialization.Mediators of inflammation · 2020Article
- Epidermal Stem Cells in Hair Follicle Cycling and Skin Regeneration: A View From the Perspective of Inflammation.Frontiers in cell and developmental biology · 2020Review
- Discovery of Exosomes From Tick Saliva and Salivary Glands Reveals Therapeutic Roles for CXCL12 and IL-8 in Wound Healing at the Tick-Human Skin Interface.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDelayed wound healing reduces the quality of life (QOL) of patients. Thus, understanding the mechanism of wound healing is indispensable for better management. However, the role of innate immunity in wound healing is thus far unknown. Recently the involvement of TLR3 in wound healing has been evaluated. The systemic administration of polyriboinosinic-polyribocytidylic acid (poly I:C ; a substitute for viral dsRNA and a ligand of toll-like receptor 3), enhances wound healing in vivo. The aim of this study is to improve our understanding of the link between innate immunity and human wound healing, particularly in re-epithelialization.
resultsThe present study showed that poly I:C significantly accelerated collective HaCaT cell migration in a scratch assay. Poly I:C also increased IL-8 and bFGF production, and anti-IL-8 antibodies significantly inhibited the migration caused by poly I:C. Human recombinant IL-8 also accelerated collective HaCaT cell migration. An immunofluorescence assay and enzyme-linked immunosorbent assay (ELISA) also revealed that poly I:C decreased E-cadherin protein levels and increased vimentin protein levels, and anti-IL-8 antibody reversed this effect. In contrast, nucleic/cytosolic protein ratios of Snail 1 were unchanged in all tested conditions.
conclusionOur findings demonstrated that poly I:C accelerated collective HaCaT cell migration via autocrine/paracrine secretions of IL-8 and the subsequent incomplete epithelial-mesenchymal transition (EMT). Our findings provide a new strategy for wound healing by regulating innate immune systems in re-epithelialization.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.