ArticleMolecular and cellular biochemistry2009
HMGb1 promotes scratch wound closure of HaCaT keratinocytes via ERK1/2 activation.
Article in Molecular and cellular biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 70 citations in OpenAlex.
- DAMP signaling networks: from receptors to diverse pathophysiological functions.Journal of advanced research · 2026Review
- The RAGE Pathway in Skin Pathology Development: A Comprehensive Review of Its Role and Therapeutic Potential.International journal of molecular sciences · 2024Review
- A novel method for the establishment of autologous skin cell suspensions: characterisation of cellular sub-populations, epidermal stem cell content and wound response-enhancing biological properties.Frontiers in bioengineering and biotechnology · 2024Article
- Perish in the Attempt: Regulated Cell Death in Regenerative and Nonregenerative Tissue.Antioxidants & redox signaling · 2023Review
- Review: The role of HMGB1 in spinal cord injury.Frontiers in immunology · 2022Review
- The Modulatory Influence of Plant-Derived Compounds on Human Keratinocyte Function.International journal of molecular sciences · 2021Review
- The extracellular innate-immune effector HMGB1 limits pathogenic bacterial biofilm proliferation.The Journal of clinical investigation · 2021Article
- The useful agent to have an ideal biological scaffold.Cell and tissue banking · 2021Review
- The Treatment of Impaired Wound Healing in Diabetes: Looking among Old Drugs.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Advanced Glycation End Products and Receptor (RAGE) Promote Wound Healing of Human Corneal Epithelial Cells.Investigative ophthalmology & visual science · 2020Article
- Restoration of calcium-induced differentiation potential and tight junction formation in HaCaT keratinocytes by functional attenuation of overexpressed high mobility group box-1 protein.Cytotechnology · 2020Article
- Targeting the Immunomodulatory CD73/Adenosine System to Improve the Therapeutic Gain of Radiotherapy.Frontiers in immunology · 2019Review
- HMGB1 deficiency reduces HJournal of cellular and molecular medicine · 2018Article
- Alerting the body to tissue injury: The role of alarmins and DAMPs in cutaneous wound healing.Current pathobiology reports · 2018Article
- Honeydew honey: biological effects on skin cells.Molecular and cellular biochemistry · 2017Article
- Poly I:C induces collective migration of HaCaT keratinocytes via IL-8.BMC immunology · 2017Article
- HMGB1 Promotes Intraoral Palatal Wound Healing through RAGE-Dependent Mechanisms.International journal of molecular sciences · 2016Article
- Mesenchymal-epithelial signalling in tumour microenvironment: role of high-mobility group Box 1.Cell and tissue research · 2016Article
- High-mobility Group Box Protein-1, Matrix Metalloproteinases, and Vitamin D in Keloids and Hypertrophic Scars.Plastic and reconstructive surgery. Global open · 2015Review
- The Roles of Growth Factors in Keratinocyte Migration.Advances in wound care · 2015Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HMGb1 is a DNA-binding protein whose role as an extracellular cytokine in inflammation and tissue regeneration has also been reported. Given the importance of keratinocytes in wound healing, we have studied the mechanism of action of HMGb1 on HaCaT keratinocytes during in vitro scratch wound repair. Western blot and confocal immunofluorescence microscopy showed that these cells express significant amounts of HMGb1, that the protein is prevalently localized in the nucleus, and that its release by cells is negligible. Western blot also showed that these cells express the HMGb1 receptor RAGE. Cell exposure to HMGb1 in the absence of serum resulted in a stimulation of cell proliferation and ERK1/2 activation. HMGb1 also accelerated the wound closure of scratch wounded cells and promoted cell migration, as evaluated by a transwell assay. The HMGb1-induced increases of cell proliferation, cell migration, and wound closure were abolished by the MEK inhibitor PD98059. Taken together, data show that, although HMGb1 is not released by HaCaT, when applied exogenously it can induce a marked increase of the wound repair of these cells. Data also suggest that HMGb1 acts via the RAGE/MEK/ERK pathway. These results bring scientific support to the potential application of HMGb1 in regenerative medicine.
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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.