Journal
PEPTIDES
Volume 76, Issue -, Pages 57-64Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.peptides.2015.12.010
Keywords
delta-Opioid receptor; Leucine-enkephalin; Wound healing; Hemidesmosome
Funding
- Gachon University Gil Medical Center [2013-41]
- Global PhD Fellowship Program [NRF-2015H1A2A1032009]
- Small and Medium Business Administration (Technological Innovation RD Program) [S2178403]
- National Research Foundation [NRF-2013R1A1A1007693, 2014K1A3A1A19066980]
- National Research Foundation of Korea [2014K1A3A1A19066980] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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The skin responds to environmental stressors by coordinated actions of neuropeptides and their receptors. An endogenous peptide for delta-opioid receptor (DOPr), Leu-enkephalin (L-ENK), is expressed in the skin and its expression is altered in pathological conditions. Although the importance of DOPr is rapidly gaining recognition, the molecular mechanisms underlying its effects on wound healing are largely undefined. We show here that L-ENK induced activation of Erk, P90(RSK) and Elk-1 and promoted the disruption of hemidesmosomes and the expression of matrix metalloprotease (MMP)-2 and MMP-9, important processes for wound healing. Treatment with Erk inhibitor blocked activation of P90(RSK) and Elk-1 and significantly blunted wound repair. Therefore, our results suggest that activation of Erk and its downstream effectors, P90(RSK) and Elk-1, are critical for DOPr-mediated skin homeostasis. (C) 2016 Elsevier Inc. All rights reserved.
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