Leucine-enkephalin promotes wound repair through the regulation of hemidesmosome dynamics and matrix metalloprotease
•L-ENK promotes wound healing in human keratinocytes.•Activation of Erk1/2, P90RSK, and Elk-1 are necessary for L-ENK-mediated wound repair.•L-ENK facilitates hemidesmosome disruption.•L-ENK increases MMP-2 and MMP-9 expression. The skin responds to environmental stressors by coordinated actions of...
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| Veröffentlicht in: | Peptides (New York, N.Y. : 1980) N.Y. : 1980), 2016-02, Vol.76, p.57-64 |
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| container_title | Peptides (New York, N.Y. : 1980) |
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| creator | Yang, Dong Joo Lee, Kyung Suk Ko, Chang Mann Moh, Sang Hyun Song, Jihyeok Hur, Lucia C. Cheon, Young Woo Yang, Seung Ho Choi, Yun-Hee Kim, Ki Woo |
| description | •L-ENK promotes wound healing in human keratinocytes.•Activation of Erk1/2, P90RSK, and Elk-1 are necessary for L-ENK-mediated wound repair.•L-ENK facilitates hemidesmosome disruption.•L-ENK increases MMP-2 and MMP-9 expression.
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. |
| doi_str_mv | 10.1016/j.peptides.2015.12.010 |
| format | Article |
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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.</description><identifier>ISSN: 0196-9781</identifier><identifier>EISSN: 1873-5169</identifier><identifier>DOI: 10.1016/j.peptides.2015.12.010</identifier><identifier>PMID: 26763532</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Abbreviations ; Activation ; Blocking ; Cell Line ; Cell Movement ; Control ; Enkephalin, Leucine - physiology ; Hemidesmosome ; Hemidesmosomes - physiology ; Humans ; Keratinocytes - physiology ; Leucine-enkephalin ; MAP Kinase Signaling System ; Matrix Metalloproteinases - metabolism ; Peptides ; Receptors ; Repair ; Wound Healing ; δ-Opioid receptor</subject><ispartof>Peptides (New York, N.Y. : 1980), 2016-02, Vol.76, p.57-64</ispartof><rights>2016 Elsevier Inc.</rights><rights>Copyright © 2016 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c401t-9a848465040398421304c467f528afbb8be58e4c4fc344ac3015f43195d76ae63</citedby><cites>FETCH-LOGICAL-c401t-9a848465040398421304c467f528afbb8be58e4c4fc344ac3015f43195d76ae63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0196978115300164$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26763532$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Dong Joo</creatorcontrib><creatorcontrib>Lee, Kyung Suk</creatorcontrib><creatorcontrib>Ko, Chang Mann</creatorcontrib><creatorcontrib>Moh, Sang Hyun</creatorcontrib><creatorcontrib>Song, Jihyeok</creatorcontrib><creatorcontrib>Hur, Lucia C.</creatorcontrib><creatorcontrib>Cheon, Young Woo</creatorcontrib><creatorcontrib>Yang, Seung Ho</creatorcontrib><creatorcontrib>Choi, Yun-Hee</creatorcontrib><creatorcontrib>Kim, Ki Woo</creatorcontrib><title>Leucine-enkephalin promotes wound repair through the regulation of hemidesmosome dynamics and matrix metalloprotease</title><title>Peptides (New York, N.Y. : 1980)</title><addtitle>Peptides</addtitle><description>•L-ENK promotes wound healing in human keratinocytes.•Activation of Erk1/2, P90RSK, and Elk-1 are necessary for L-ENK-mediated wound repair.•L-ENK facilitates hemidesmosome disruption.•L-ENK increases MMP-2 and MMP-9 expression.
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.</description><subject>Abbreviations</subject><subject>Activation</subject><subject>Blocking</subject><subject>Cell Line</subject><subject>Cell Movement</subject><subject>Control</subject><subject>Enkephalin, Leucine - physiology</subject><subject>Hemidesmosome</subject><subject>Hemidesmosomes - physiology</subject><subject>Humans</subject><subject>Keratinocytes - physiology</subject><subject>Leucine-enkephalin</subject><subject>MAP Kinase Signaling System</subject><subject>Matrix Metalloproteinases - metabolism</subject><subject>Peptides</subject><subject>Receptors</subject><subject>Repair</subject><subject>Wound Healing</subject><subject>δ-Opioid receptor</subject><issn>0196-9781</issn><issn>1873-5169</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU9v1DAQxS0EotvCV6h85JJ0HDuOcyuq-FNpJS5wtrzOpOsljlPbge63x6ttufY00ui9eaP3I-SaQc2AyZtDveCS3YCpboC1NWtqYPCGbJjqeNUy2b8lG2C9rPpOsQtymdIBAITo1Xty0chO8pY3G5K3uFo3Y4Xzb1z2ZnIzXWLwIWOif8M6DzTiYlykeR_D-rAvE8vqYZ1MdmGmYaR79KdHfEjBIx2Os_HOJmqK15sc3RP1mM00hXI4o0n4gbwbzZTw4_O8Ir--fvl5973a_vh2f_d5W1kBLFe9UUIJ2YIA3ivRMA7CCtmNbaPMuNupHbYKy2q0XAhjeSliFJz17dBJg5JfkU_nuyX4ccWUtXfJ4jSZGcOaNFNMgoRG9K9LOym4ANmdpPIstTGkFHHUS3TexKNmoE9w9EG_wNEnOJo1usApxuvnjHXncfhve6FRBLdnAZZS_jiMOlmHs8XBRbRZD8G9lvEPwMmluQ</recordid><startdate>201602</startdate><enddate>201602</enddate><creator>Yang, Dong Joo</creator><creator>Lee, Kyung Suk</creator><creator>Ko, Chang Mann</creator><creator>Moh, Sang Hyun</creator><creator>Song, Jihyeok</creator><creator>Hur, Lucia C.</creator><creator>Cheon, Young Woo</creator><creator>Yang, Seung Ho</creator><creator>Choi, Yun-Hee</creator><creator>Kim, Ki Woo</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7U5</scope><scope>8FD</scope><scope>L7M</scope></search><sort><creationdate>201602</creationdate><title>Leucine-enkephalin promotes wound repair through the regulation of hemidesmosome dynamics and matrix metalloprotease</title><author>Yang, Dong Joo ; Lee, Kyung Suk ; Ko, Chang Mann ; Moh, Sang Hyun ; Song, Jihyeok ; Hur, Lucia C. ; Cheon, Young Woo ; Yang, Seung Ho ; Choi, Yun-Hee ; Kim, Ki Woo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c401t-9a848465040398421304c467f528afbb8be58e4c4fc344ac3015f43195d76ae63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Abbreviations</topic><topic>Activation</topic><topic>Blocking</topic><topic>Cell Line</topic><topic>Cell Movement</topic><topic>Control</topic><topic>Enkephalin, Leucine - physiology</topic><topic>Hemidesmosome</topic><topic>Hemidesmosomes - physiology</topic><topic>Humans</topic><topic>Keratinocytes - physiology</topic><topic>Leucine-enkephalin</topic><topic>MAP Kinase Signaling System</topic><topic>Matrix Metalloproteinases - metabolism</topic><topic>Peptides</topic><topic>Receptors</topic><topic>Repair</topic><topic>Wound Healing</topic><topic>δ-Opioid receptor</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Dong Joo</creatorcontrib><creatorcontrib>Lee, Kyung Suk</creatorcontrib><creatorcontrib>Ko, Chang Mann</creatorcontrib><creatorcontrib>Moh, Sang Hyun</creatorcontrib><creatorcontrib>Song, Jihyeok</creatorcontrib><creatorcontrib>Hur, Lucia C.</creatorcontrib><creatorcontrib>Cheon, Young Woo</creatorcontrib><creatorcontrib>Yang, Seung Ho</creatorcontrib><creatorcontrib>Choi, Yun-Hee</creatorcontrib><creatorcontrib>Kim, Ki Woo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>Technology Research Database</collection><collection>Advanced Technologies Database with Aerospace</collection><jtitle>Peptides (New York, N.Y. : 1980)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Dong Joo</au><au>Lee, Kyung Suk</au><au>Ko, Chang Mann</au><au>Moh, Sang Hyun</au><au>Song, Jihyeok</au><au>Hur, Lucia C.</au><au>Cheon, Young Woo</au><au>Yang, Seung Ho</au><au>Choi, Yun-Hee</au><au>Kim, Ki Woo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Leucine-enkephalin promotes wound repair through the regulation of hemidesmosome dynamics and matrix metalloprotease</atitle><jtitle>Peptides (New York, N.Y. : 1980)</jtitle><addtitle>Peptides</addtitle><date>2016-02</date><risdate>2016</risdate><volume>76</volume><spage>57</spage><epage>64</epage><pages>57-64</pages><issn>0196-9781</issn><eissn>1873-5169</eissn><abstract>•L-ENK promotes wound healing in human keratinocytes.•Activation of Erk1/2, P90RSK, and Elk-1 are necessary for L-ENK-mediated wound repair.•L-ENK facilitates hemidesmosome disruption.•L-ENK increases MMP-2 and MMP-9 expression.
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.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>26763532</pmid><doi>10.1016/j.peptides.2015.12.010</doi><tpages>8</tpages></addata></record> |
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| subjects | Abbreviations Activation Blocking Cell Line Cell Movement Control Enkephalin, Leucine - physiology Hemidesmosome Hemidesmosomes - physiology Humans Keratinocytes - physiology Leucine-enkephalin MAP Kinase Signaling System Matrix Metalloproteinases - metabolism Peptides Receptors Repair Wound Healing δ-Opioid receptor |
| title | Leucine-enkephalin promotes wound repair through the regulation of hemidesmosome dynamics and matrix metalloprotease |
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