ArticleThe Journal of investigative dermatology2009
Wounding-induced synthesis of hyaluronic acid in organotypic epidermal cultures requires the release of heparin-binding egf and activation of the EGFR.
Article in The Journal of investigative dermatology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 49 citations in OpenAlex.
- Treatment and Improvement of Healing after Surgical Intervention.Healthcare (Basel, Switzerland) · 2023Review
- Review
- A biophysically-defined hyaluronic acid-based compound accelerates migration and stimulates the production of keratinocyte-derived neuromodulators.Cell adhesion & migration · 2019Article
- Heparin-Binding Epidermal Growth Factor-Like Growth Factor as a Critical Mediator of Tissue Repair and Regeneration.The American journal of pathology · 2018Review
- Brain extracellular space, hyaluronan, and the prevention of epileptic seizures.Reviews in the neurosciences · 2017Review
- Human Keratinocytes Respond to Extracellular UTP by Induction of Hyaluronan Synthase 2 Expression and Increased Hyaluronan Synthesis.The Journal of biological chemistry · 2017Article
- Hyaluronan: More than just a wrinkle filler.Glycobiology · 2016Review
- Hyaluronan - a functional and structural sweet spot in the tissue microenvironment.Frontiers in immunology · 2015Review
- Roles of Proteoglycans and Glycosaminoglycans in Wound Healing and Fibrosis.International journal of cell biology · 2015Review
- Modeling vitamin D actions in triple negative/basal-like breast cancer.The Journal of steroid biochemistry and molecular biology · 2014Review
- Hyaluronan metabolism in human keratinocytes and atopic dermatitis skin is driven by a balance of hyaluronan synthases 1 and 3.The Journal of investigative dermatology · 2014Article
- Extracellular UDP-glucose activates P2Y14 Receptor and Induces Signal Transducer and Activator of Transcription 3 (STAT3) Tyr705 phosphorylation and binding to hyaluronan synthase 2 (HAS2) promoter, stimulating hyaluronan synthesis of keratinocytes.The Journal of biological chemistry · 2014Article
- Hyaluronan-phosphatidylethanolamine polymers form pericellular coats on keratinocytes and promote basal keratinocyte proliferation.BioMed research international · 2014Article
- Low dose ultraviolet B irradiation increases hyaluronan synthesis in epidermal keratinocytes via sequential induction of hyaluronan synthases Has1-3 mediated by p38 and Ca2+/calmodulin-dependent protein kinase II (CaMKII) signaling.The Journal of biological chemistry · 2013Article
- Regenerative potential of glycosaminoglycans for skin and bone.Journal of molecular medicine (Berlin, Germany) · 2012Review
- Adipose-derived stromal cells accelerate wound healing in an organotypic raft culture model.Annals of plastic surgery · 2012Article
- Enhanced inflammation and accelerated wound closure following tetraphorbol ester application or full-thickness wounding in mice lacking hyaluronan synthases Has1 and Has3.The Journal of investigative dermatology · 2012Article
- Receptor for hyaluronan-mediated motility isoform B promotes liver metastasis in a mouse model of multistep tumorigenesis and a tail vein assay for metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Hyaluronan matrices in pathobiological processes.The FEBS journal · 2011Review
- Novel regulation and dynamics of myosin II activation during epidermal wound responses.Experimental cell research · 2010Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Hyaluronic acid (HA), a glycosaminoglycan located between keratinocytes in the epidermis, accumulates dramatically following skin wounding. To study inductive mechanisms, a rat keratinocyte organotypic culture model that faithfully mimics HA metabolism was used. Organotypic cultures were needle-punctured 100 times, incubated for up to 24 hours, and HA analyzed by histochemical and biochemical methods. Within 15 minutes post-injury, HA levels had elevated two-fold, increasing to four-fold by 24 hours. HA elevations far from the site of injury suggested the possible involvement of a soluble HA-inductive factor. Media transfer experiments (from wounded cultures to unwounded cultures) confirmed the existence of a soluble factor. From earlier evidence, we hypothesized that an EGF-like growth factor might be responsible. This was confirmed as follows: (1) EGFR kinase inhibitor (AG1478) completely prevented wounding-induced HA accumulation. (2) Rapid tyrosine-phosphorylation of EGFR correlated well with the onset of increased HA synthesis. (3) A neutralizing antibody that recognizes heparin binding EGF-like growth factor (HB-EGF) blocked wounding-induced HA synthesis by > or =50%. (4) Western analyses showed that release of activated HB-EGF (but neither amphiregulin nor EGF) occured after wounding. In summary, rapid HA accumulation after epidermal wounding occurs through a mechanism requiring cleavage of HB-EGF and activation of EGFR signaling.
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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.