Leucine-enkephalin promotes wound repair through the regulation of hemidesmosome dynamics and matrix metalloprotease

Dong Joo Yang; Kyung Suk Lee; Chang Mann Ko; Sang Hyun Moh; Jihyeok Song; Lucia C. Hur; Young Woo Cheon; Seung Ho Yang; Yun Hee Choi; Ki Woo Kim

doi:10.1016/j.peptides.2015.12.010

Leucine-enkephalin promotes wound repair through the regulation of hemidesmosome dynamics and matrix metalloprotease

Dong Joo Yang, Kyung Suk Lee, Chang Mann Ko, Sang Hyun Moh, Jihyeok Song, Lucia C. Hur, Young Woo Cheon, Seung Ho Yang, Yun Hee Choi, Ki Woo Kim

Department of Oral Biology

Research output: Contribution to journal › Article › peer-review

13 Citations (Scopus)

Abstract

The skin responds to environmental stressors by coordinated actions of neuropeptides and their receptors. An endogenous peptide for δ-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.

Original language	English
Pages (from-to)	57-64
Number of pages	8
Journal	Peptides
Volume	76
DOIs	https://doi.org/10.1016/j.peptides.2015.12.010
Publication status	Published - 2016 Feb

Bibliographical note

Funding Information:
We would like to thank Ann W. Kinyua (Yonsei University) for the critical reading of this manuscript. This research was supported by Gachon University Gil Medical Center Grant 2013-41 for Y.W.C., Global PhD Fellowship Program ( NRF-2015H1A2A1032009 ) for D.J.Y., Small and Medium Business Administration (Technological Innovation R&D Program S2178403 ) for S.H.M., and the National Research Foundation ( NRF-2013R1A1A1007693 and 2014K1A3A1A19066980 ) for K.W.K.

Publisher Copyright:
© 2016 Elsevier Inc. All rights reserved.

All Science Journal Classification (ASJC) codes

Biochemistry
Physiology
Endocrinology
Cellular and Molecular Neuroscience

Access to Document

10.1016/j.peptides.2015.12.010

Cite this

@article{717ae9462d114271806a30ab72111654,

title = "Leucine-enkephalin promotes wound repair through the regulation of hemidesmosome dynamics and matrix metalloprotease",

abstract = "The skin responds to environmental stressors by coordinated actions of neuropeptides and their receptors. An endogenous peptide for δ-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, P90RSK, 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 P90RSK and Elk-1 and significantly blunted wound repair. Therefore, our results suggest that activation of Erk and its downstream effectors, P90RSK and Elk-1, are critical for DOPr-mediated skin homeostasis.",

author = "Yang, {Dong Joo} and Lee, {Kyung Suk} and Ko, {Chang Mann} and Moh, {Sang Hyun} and Jihyeok Song and Hur, {Lucia C.} and Cheon, {Young Woo} and Yang, {Seung Ho} and Choi, {Yun Hee} and Kim, {Ki Woo}",

note = "Funding Information: We would like to thank Ann W. Kinyua (Yonsei University) for the critical reading of this manuscript. This research was supported by Gachon University Gil Medical Center Grant 2013-41 for Y.W.C., Global PhD Fellowship Program ( NRF-2015H1A2A1032009 ) for D.J.Y., Small and Medium Business Administration (Technological Innovation R&D Program S2178403 ) for S.H.M., and the National Research Foundation ( NRF-2013R1A1A1007693 and 2014K1A3A1A19066980 ) for K.W.K. Publisher Copyright: {\textcopyright} 2016 Elsevier Inc. All rights reserved.",

year = "2016",

month = feb,

doi = "10.1016/j.peptides.2015.12.010",

language = "English",

volume = "76",

pages = "57--64",

journal = "Peptides",

issn = "0196-9781",

publisher = "Elsevier Inc.",

}

TY - JOUR

T1 - Leucine-enkephalin promotes wound repair through the regulation of hemidesmosome dynamics and matrix metalloprotease

AU - Yang, Dong Joo

AU - Lee, Kyung Suk

AU - Ko, Chang Mann

AU - Moh, Sang Hyun

AU - Song, Jihyeok

AU - Hur, Lucia C.

AU - Cheon, Young Woo

AU - Yang, Seung Ho

AU - Choi, Yun Hee

AU - Kim, Ki Woo

N1 - Funding Information: We would like to thank Ann W. Kinyua (Yonsei University) for the critical reading of this manuscript. This research was supported by Gachon University Gil Medical Center Grant 2013-41 for Y.W.C., Global PhD Fellowship Program ( NRF-2015H1A2A1032009 ) for D.J.Y., Small and Medium Business Administration (Technological Innovation R&D Program S2178403 ) for S.H.M., and the National Research Foundation ( NRF-2013R1A1A1007693 and 2014K1A3A1A19066980 ) for K.W.K. Publisher Copyright: © 2016 Elsevier Inc. All rights reserved.

PY - 2016/2

Y1 - 2016/2

N2 - The skin responds to environmental stressors by coordinated actions of neuropeptides and their receptors. An endogenous peptide for δ-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, P90RSK, 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 P90RSK and Elk-1 and significantly blunted wound repair. Therefore, our results suggest that activation of Erk and its downstream effectors, P90RSK and Elk-1, are critical for DOPr-mediated skin homeostasis.

AB - The skin responds to environmental stressors by coordinated actions of neuropeptides and their receptors. An endogenous peptide for δ-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, P90RSK, 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 P90RSK and Elk-1 and significantly blunted wound repair. Therefore, our results suggest that activation of Erk and its downstream effectors, P90RSK and Elk-1, are critical for DOPr-mediated skin homeostasis.

UR - http://www.scopus.com/inward/record.url?scp=84954289890&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84954289890&partnerID=8YFLogxK

U2 - 10.1016/j.peptides.2015.12.010

DO - 10.1016/j.peptides.2015.12.010

M3 - Article

C2 - 26763532

AN - SCOPUS:84954289890

SN - 0196-9781

VL - 76

SP - 57

EP - 64

JO - Peptides

JF - Peptides

ER -

Leucine-enkephalin promotes wound repair through the regulation of hemidesmosome dynamics and matrix metalloprotease

Abstract

Bibliographical note

All Science Journal Classification (ASJC) codes

Access to Document

Other files and links

Fingerprint

Cite this