{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Kim CS"],"funding":["National Institute of General Medical Sciences","Division of Chemical, Bioengineering, Environmental, and Transport Systems","NIGMS NIH HHS"],"pagination":["e10138"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6764804"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["4(3)"],"pubmed_abstract":["Re-epithelialization is a critical step in wound healing and results from the collective migration of keratinocytes. Previous work demonstrated that immobilized, but not soluble, epidermal growth factor (EGF) resulted in leader cell-specific activation of phospholipase C gamma 1 (PLCγ1) in HaCaT keratinocytes, and that this PLCγ1 activation was necessary to drive persistent cell migration. To determine the mechanism responsible for wound edge-localized PLCγ1 activation, we examined differences in cell area, cell-cell interactions, and EGF receptor (EGFR) localization between wound edge and bulk cells treated with vehicle, soluble EGF, or immobilized EGF. Our results support a multistep mechanism where EGFR translocation from the lateral membrane to the basolateral/basal membrane allows clustering in response to immobilized EGF. This analysis of factors regulating PLCγ1 activation is a crucial step toward developing therapies or wound dressings capable of modulating this signal and, consequently, cell migration."],"journal":["Bioengineering & translational medicine"],"pubmed_title":["Leader cell PLCγ1 activation during keratinocyte collective migration is induced by EGFR localization and clustering."],"pmcid":["PMC6764804"],"funding_grant_id":["CBET‐1401584","R01GM099031","R01 GM099031"],"pubmed_authors":["Yang X","Kim CS","Masters KS","Kreeger PK","Jacobsen S"],"additional_accession":[]},"is_claimable":false,"name":"Leader cell PLCγ1 activation during keratinocyte collective migration is induced by EGFR localization and clustering.","description":"Re-epithelialization is a critical step in wound healing and results from the collective migration of keratinocytes. Previous work demonstrated that immobilized, but not soluble, epidermal growth factor (EGF) resulted in leader cell-specific activation of phospholipase C gamma 1 (PLCγ1) in HaCaT keratinocytes, and that this PLCγ1 activation was necessary to drive persistent cell migration. To determine the mechanism responsible for wound edge-localized PLCγ1 activation, we examined differences in cell area, cell-cell interactions, and EGF receptor (EGFR) localization between wound edge and bulk cells treated with vehicle, soluble EGF, or immobilized EGF. Our results support a multistep mechanism where EGFR translocation from the lateral membrane to the basolateral/basal membrane allows clustering in response to immobilized EGF. This analysis of factors regulating PLCγ1 activation is a crucial step toward developing therapies or wound dressings capable of modulating this signal and, consequently, cell migration.","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Sep","modification":"2025-04-21T23:23:36.989Z","creation":"2019-10-11T07:12:13Z"},"accession":"S-EPMC6764804","cross_references":{"pubmed":["31572796"],"doi":["10.1002/btm2.10138"]}}