Adrenergic signaling in human oral keratinocytes and wound repair.

Abstract:

:Catecholamines are present in saliva, but their influence on oral epithelium is not understood. Because psychological stress increases salivary catecholamines and impairs oral mucosal wound healing, we sought to determine if epithelial adrenergic signaling could link these two findings. We found that cultured human oral keratinocytes (HOK) express the α(2B)- and β(2)-adrenergic receptors (ARs). Exposure of HOK to either epinephrine or the β-AR agonist, isoproterenol, reduced migratory speed and decreased in vitro scratch wound healing. Incubation with the β-AR antagonist timolol reversed the catecholamine-induced effects, indicating that the observed response is mediated by β-AR. Epinephrine treatment decreased phosphorylation of the mitogen-activated protein kinases (MAPK) ERK1/2 and p38; these decreases were also reversed with timolol. Cultured HOK express enzymes of the epinephrine synthetic pathway, and generate epinephrine. These findings demonstrate that stress-induced elevations of salivary catecholamines signal through MAPK pathways, and result in impaired oral keratinocyte migration required for healing.

journal_name

J Dent Res

authors

Steenhuis P,Huntley RE,Gurenko Z,Yin L,Dale BA,Fazel N,Isseroff RR

doi

10.1177/0022034510388034

subject

Has Abstract

pub_date

2011-02-01 00:00:00

pages

186-92

issue

2

eissn

0022-0345

issn

1544-0591

pii

0022034510388034

journal_volume

90

pub_type

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