Leader cell PLCγ1 activation during keratinocyte collective migration is induced by EGFR localization and clustering.

immobilized growth factor receptor clustering re‐epithelialization wound healing

Journal

Bioengineering & translational medicine
ISSN: 2380-6761
Titre abrégé: Bioeng Transl Med
Pays: United States
ID NLM: 101689146

Informations de publication

Date de publication:
Sep 2019
Historique:
received: 14 04 2019
revised: 14 06 2019
accepted: 17 06 2019
entrez: 2 10 2019
pubmed: 2 10 2019
medline: 2 10 2019
Statut: epublish

Résumé

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.

Identifiants

pubmed: 31572796
doi: 10.1002/btm2.10138
pii: BTM210138
pmc: PMC6764804
doi:

Types de publication

Journal Article

Langues

eng

Pagination

e10138

Subventions

Organisme : NIGMS NIH HHS
ID : R01 GM099031
Pays : United States

Informations de copyright

© 2019 The Authors. Bioengineering & Translational Medicine published by Wiley Periodicals, Inc. on behalf of The American Institute of Chemical Engineers.

Déclaration de conflit d'intérêts

The authors declare no competing financial interests.

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Auteurs

Chloe S Kim (CS)

Department of Biomedical Engineering University of Wisconsin-Madison Madison WI 53705.

Xinhai Yang (X)

Department of Biomedical Engineering University of Wisconsin-Madison Madison WI 53705.

Sarah Jacobsen (S)

Department of Biomedical Engineering University of Wisconsin-Madison Madison WI 53705.

Kristyn S Masters (KS)

Department of Biomedical Engineering University of Wisconsin-Madison Madison WI 53705.
Carbone Cancer Center University of Wisconsin School of Medicine and Public Health Madison WI 53705.
Department of Medicine University of Wisconsin School of Medicine and Public Health Madison WI 53705.

Pamela K Kreeger (PK)

Department of Biomedical Engineering University of Wisconsin-Madison Madison WI 53705.
Carbone Cancer Center University of Wisconsin School of Medicine and Public Health Madison WI 53705.
Department of Cell and Regenerative Biology University of Wisconsin School of Medicine and Public Health Madison WI 53705.

Classifications MeSH