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Updated: Oct 30, 2025
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A Novel In Vitro Wound Healing Assay to Evaluate Cell Migration
Published on: March 17, 2018
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Alpha and beta adrenergic receptors modulate keratinocyte migration
Hsin-Ya Yang1, Pieter Steenhuis1, Aaron M Glucksman1
1Department of Dermatology, University of California, Davis, Davis, California, United States of America.
Plos One
|July 2, 2021
Summary
Low epinephrine concentrations paradoxically increase skin keratinocyte migration via alpha-2B-adrenergic receptors (A2B-AR), suggesting a novel regulatory role in wound healing beyond beta-2-adrenergic receptors (B2AR).
Area of Science:
- Dermatology
- Cell Biology
- Pharmacology
Background:
- Keratinocyte migration is crucial for wound healing and closure.
- Beta-2-adrenergic receptors (B2AR) activation by high epinephrine levels impairs keratinocyte migration and delays wound healing.
Purpose of the Study:
- To investigate the paradoxical effect of low epinephrine concentrations on keratinocyte migration.
- To identify the adrenergic receptor subtypes involved in mediating epinephrine's effect on keratinocyte migration.
Main Methods:
- Human keratinocyte strains were exposed to varying epinephrine concentrations (0.1 nM vs 1 μM).
- Specific alpha-adrenergic receptor (alpha-AR) inhibitors were used to block receptor activity.
- ERK phosphorylation levels were measured following epinephrine treatment and receptor blockade.
Main Results:
- Low epinephrine (0.1 nM) concentrations increased keratinocyte migration in a subset of cell strains.
- Human keratinocytes express both alpha- and beta-adrenergic receptors, including alpha-2 AR subtypes.
- Blocking alpha-2B-adrenergic receptors (A2B-AR) reversed the enhanced migration induced by low epinephrine.
- Low epinephrine increased ERK phosphorylation, which was inhibited by A2B-AR blockade.
Conclusions:
- Both A2B-AR and B2AR mediate keratinocyte migration.
- A2B-AR plays a novel role in regulating keratinocyte migration, potentially by modulating B2AR signaling at low epinephrine concentrations.
- Findings suggest a complex adrenergic receptor-mediated regulation of skin wound healing.
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