ArticleThe American journal of pathology2011
Distinct activation of epidermal growth factor receptor by UTP contributes to epithelial cell wound repair.
Article in The American journal of pathology, 2011. 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, 26 citations in OpenAlex.
- Nuclear IL-33 Plays an Important Role in EGFR-Mediated Keratinocyte Migration by Regulating the Activation of Signal Transducer and Activator of Transcription 3 and NF-κB.JID innovations : skin science from molecules to population health · 2023Article
- TNFα promotes mucosal wound repair through enhanced platelet activating factor receptor signaling in the epithelium.Mucosal immunology · 2019Article
- P2YCirculation research · 2017Article
- Purinergic Signaling in Corneal Wound Healing: A Tale of 2 Receptors.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2016Review
- Progress in corneal wound healing.Progress in retinal and eye research · 2015Review
- Purines in the eye: recent evidence for the physiological and pathological role of purines in the RPE, retinal neurons, astrocytes, Müller cells, lens, trabecular meshwork, cornea and lacrimal gland.Experimental eye research · 2014Review
- P2Y2 nucleotide receptor activation enhances the aggregation and self-organization of dispersed salivary epithelial cells.American journal of physiology. Cell physiology · 2014Article
- STRAP PTM: Software Tool for Rapid Annotation and Differential Comparison of Protein Post-Translational Modifications.Current protocols in bioinformatics · 2013Article
- Epithelial wounds induce differential phosphorylation changes in response to purinergic and EGF receptor activation.The American journal of pathology · 2013Article
- A comparison of epithelial-to-mesenchymal transition and re-epithelialization.Seminars in cancer biology · 2012Review
- Communication between corneal epithelial cells and trigeminal neurons is facilitated by purinergic (P2) and glutamatergic receptors.PloS one · 2012Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The release of nucleotides after injury activates purinergic receptors, leading to phosphorylation of site-specific residues on epidermal growth factor receptor (EGFR). To elucidate the differences between the injury-induced response and that induced by exogenous EGF, we examined recruitment of docking proteins, internalization of EGFR, and migration after injury. Injury induced by scratch wounds or stimulation by addition of UTP caused a brief internalization of EGFR, which paralleled the lesser association with growth factor receptor-bound protein 2 (Grb2) and phosphorylation of EGFR. The internalization caused by EGF was sustained and detected for longer than 60 minutes and correlated with phosphorylation of the receptor. The EGF caused recruitment of Grb2, phospholipase C-γ-1 (PLCγ1), Shc, and Src to EGFR. Glutathione S-transferase pull downs were performed, and glutathione S-transferase-PLCγ1 showed binding of Grb2 when stimulated with EGF but not with UTP or injury. Furthermore, UTP did not induce PLCγ1 phosphorylation, and the phosphorylation induced by EGF was attenuated by costimulation with UTP. The response to heparin-binding EGF was equivalent to that of EGF. Site-directed mutagenesis showed that phosphorylation of Y1068 and Y1086 of EGFR is required for repair. Together, our results show that injury and activation of purinergic receptors and direct activation of EGFR via EGF induce distinct downstream pathways.
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Registered trials
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