Making sense of hypertrophic scar: a role for nerves
ABSTRACT Healed partial thickness wounds including burns and donor sites cause hypertrophic scar formation and patient discomfort. For many patients with hypertrophic scars, pruritis is the most distressing symptom, which leads to wound excoriation and chronic wound formation. In spite of the clinic...
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description | ABSTRACT
Healed partial thickness wounds including burns and donor sites cause hypertrophic scar formation and patient discomfort. For many patients with hypertrophic scars, pruritis is the most distressing symptom, which leads to wound excoriation and chronic wound formation. In spite of the clinical significance of abnormal innervation in scars, the nervous system has been largely ignored in the pathophysiology of hypertrophic scars. Evidence that neuropeptides contribute to inflammatory responses to injury include inflammatory cell chemotaxis, cytokine and growth factor production. The neuropeptide substance P, which is released from nerve endings after injury, induces inflammation and mediates angiogenesis, keratinocyte proliferation, and fibrogenesis. Substance P activity is tightly regulated by neutral endopeptidase (NEP), a membrane bound metallopeptidase that degrades substance P at the cell membrane. Altered substance P levels may contribute to impaired cutaneous healing responses associated with diabetes mellitus or hypertrophic scar formation. Topical application of exogenous substance P or an NEP inhibitor enhances wound closure kinetics in diabetic murine wounds suggesting that diabetic wounds have insufficient substance P levels to promote a neuroinflammatory response necessary for normal wound repair. Conversely, increased nerve numbers and neuropeptide levels with reduced NEP levels in human and porcine hypertrophic scar samples suggest that excessive neuropeptide activity induces exuberant inflammation in hypertrophic scars. Given these observations about the role of neuropeptides in cutaneous repair, neuronal modulation of repair processes at two extremes of abnormal wound healing, chronic non‐healing ulcers in type II diabetes mellitus and hypertrophic scars in deep partial thickness wounds, may provide therapeutic targets. |
doi_str_mv | 10.1111/j.1524-475X.2007.00222.x |
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Healed partial thickness wounds including burns and donor sites cause hypertrophic scar formation and patient discomfort. For many patients with hypertrophic scars, pruritis is the most distressing symptom, which leads to wound excoriation and chronic wound formation. In spite of the clinical significance of abnormal innervation in scars, the nervous system has been largely ignored in the pathophysiology of hypertrophic scars. Evidence that neuropeptides contribute to inflammatory responses to injury include inflammatory cell chemotaxis, cytokine and growth factor production. The neuropeptide substance P, which is released from nerve endings after injury, induces inflammation and mediates angiogenesis, keratinocyte proliferation, and fibrogenesis. Substance P activity is tightly regulated by neutral endopeptidase (NEP), a membrane bound metallopeptidase that degrades substance P at the cell membrane. Altered substance P levels may contribute to impaired cutaneous healing responses associated with diabetes mellitus or hypertrophic scar formation. Topical application of exogenous substance P or an NEP inhibitor enhances wound closure kinetics in diabetic murine wounds suggesting that diabetic wounds have insufficient substance P levels to promote a neuroinflammatory response necessary for normal wound repair. Conversely, increased nerve numbers and neuropeptide levels with reduced NEP levels in human and porcine hypertrophic scar samples suggest that excessive neuropeptide activity induces exuberant inflammation in hypertrophic scars. Given these observations about the role of neuropeptides in cutaneous repair, neuronal modulation of repair processes at two extremes of abnormal wound healing, chronic non‐healing ulcers in type II diabetes mellitus and hypertrophic scars in deep partial thickness wounds, may provide therapeutic targets.</description><identifier>ISSN: 1067-1927</identifier><identifier>EISSN: 1524-475X</identifier><identifier>DOI: 10.1111/j.1524-475X.2007.00222.x</identifier><identifier>PMID: 17727464</identifier><language>eng</language><publisher>Malden, USA: Blackwell Publishing Inc</publisher><subject>Animals ; Burns - physiopathology ; Cicatrix, Hypertrophic - physiopathology ; Endopeptidases - physiology ; Humans ; Neuropeptides - blood ; Neuropeptides - physiology ; Peripheral Nerves - physiology ; Proprioception - physiology ; Protease Inhibitors - pharmacology ; Substance P - blood ; Substance P - physiology ; Wound Healing - physiology</subject><ispartof>Wound repair and regeneration, 2007-09, Vol.15 (s1), p.S27-S31</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5012-5e471a034a67086e3b77c0189b56b790448c191a9ee5a604a3a0939cda7c4d03</citedby><cites>FETCH-LOGICAL-c5012-5e471a034a67086e3b77c0189b56b790448c191a9ee5a604a3a0939cda7c4d03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1524-475X.2007.00222.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1524-475X.2007.00222.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17727464$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Scott, Jeffrey R.</creatorcontrib><creatorcontrib>Muangman, Pornprom</creatorcontrib><creatorcontrib>Gibran, Nicole S.</creatorcontrib><title>Making sense of hypertrophic scar: a role for nerves</title><title>Wound repair and regeneration</title><addtitle>Wound Repair Regen</addtitle><description>ABSTRACT
Healed partial thickness wounds including burns and donor sites cause hypertrophic scar formation and patient discomfort. For many patients with hypertrophic scars, pruritis is the most distressing symptom, which leads to wound excoriation and chronic wound formation. In spite of the clinical significance of abnormal innervation in scars, the nervous system has been largely ignored in the pathophysiology of hypertrophic scars. Evidence that neuropeptides contribute to inflammatory responses to injury include inflammatory cell chemotaxis, cytokine and growth factor production. The neuropeptide substance P, which is released from nerve endings after injury, induces inflammation and mediates angiogenesis, keratinocyte proliferation, and fibrogenesis. Substance P activity is tightly regulated by neutral endopeptidase (NEP), a membrane bound metallopeptidase that degrades substance P at the cell membrane. Altered substance P levels may contribute to impaired cutaneous healing responses associated with diabetes mellitus or hypertrophic scar formation. Topical application of exogenous substance P or an NEP inhibitor enhances wound closure kinetics in diabetic murine wounds suggesting that diabetic wounds have insufficient substance P levels to promote a neuroinflammatory response necessary for normal wound repair. Conversely, increased nerve numbers and neuropeptide levels with reduced NEP levels in human and porcine hypertrophic scar samples suggest that excessive neuropeptide activity induces exuberant inflammation in hypertrophic scars. Given these observations about the role of neuropeptides in cutaneous repair, neuronal modulation of repair processes at two extremes of abnormal wound healing, chronic non‐healing ulcers in type II diabetes mellitus and hypertrophic scars in deep partial thickness wounds, may provide therapeutic targets.</description><subject>Animals</subject><subject>Burns - physiopathology</subject><subject>Cicatrix, Hypertrophic - physiopathology</subject><subject>Endopeptidases - physiology</subject><subject>Humans</subject><subject>Neuropeptides - blood</subject><subject>Neuropeptides - physiology</subject><subject>Peripheral Nerves - physiology</subject><subject>Proprioception - physiology</subject><subject>Protease Inhibitors - pharmacology</subject><subject>Substance P - blood</subject><subject>Substance P - physiology</subject><subject>Wound Healing - physiology</subject><issn>1067-1927</issn><issn>1524-475X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkMtOAjEUQBujEV-_YLpyN-Ntp4-pcWN8oAlqYkh015RykYGBwRYU_t4ZIbjUbnqTnnObHEIog5TV53yUMslFIrR8SzmATgE45-lyhxxsH3brGZROmOG6RQ5jHAGAlCbfJy2mNddCiQMiHt24mL7TiNOItBrQ4WqGYR6q2bDwNHoXLqijoSqRDqpApxg-MR6TvYErI55s7iPSvbvtXt8nnef2w_VVJ_ESGE8kCs0cZMIpDbnCrKe1B5abnlQ9bUCI3DPDnEGUToFwmQOTGd932os-ZEfkbL12FqqPBca5nRTRY1m6KVaLaFXOmciV-hPkYOo8sgHzNehDFWPAgZ2FYuLCyjKwTVk7sk1A2wS0TVn7U9Yua_V088eiN8H-r7hJWQOXa-CrKHH178X29eWlHmo9WetFnONyq7swtkpnWtrXp7bNuOqwm3tju9k3jV6T5g</recordid><startdate>200709</startdate><enddate>200709</enddate><creator>Scott, Jeffrey R.</creator><creator>Muangman, Pornprom</creator><creator>Gibran, Nicole S.</creator><general>Blackwell Publishing Inc</general><scope>BSCLL</scope><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>7TK</scope><scope>7X8</scope></search><sort><creationdate>200709</creationdate><title>Making sense of hypertrophic scar: a role for nerves</title><author>Scott, Jeffrey R. ; Muangman, Pornprom ; Gibran, Nicole S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5012-5e471a034a67086e3b77c0189b56b790448c191a9ee5a604a3a0939cda7c4d03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Burns - physiopathology</topic><topic>Cicatrix, Hypertrophic - physiopathology</topic><topic>Endopeptidases - physiology</topic><topic>Humans</topic><topic>Neuropeptides - blood</topic><topic>Neuropeptides - physiology</topic><topic>Peripheral Nerves - physiology</topic><topic>Proprioception - physiology</topic><topic>Protease Inhibitors - pharmacology</topic><topic>Substance P - blood</topic><topic>Substance P - physiology</topic><topic>Wound Healing - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Scott, Jeffrey R.</creatorcontrib><creatorcontrib>Muangman, Pornprom</creatorcontrib><creatorcontrib>Gibran, Nicole S.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Wound repair and regeneration</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Scott, Jeffrey R.</au><au>Muangman, Pornprom</au><au>Gibran, Nicole S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Making sense of hypertrophic scar: a role for nerves</atitle><jtitle>Wound repair and regeneration</jtitle><addtitle>Wound Repair Regen</addtitle><date>2007-09</date><risdate>2007</risdate><volume>15</volume><issue>s1</issue><spage>S27</spage><epage>S31</epage><pages>S27-S31</pages><issn>1067-1927</issn><eissn>1524-475X</eissn><abstract>ABSTRACT
Healed partial thickness wounds including burns and donor sites cause hypertrophic scar formation and patient discomfort. For many patients with hypertrophic scars, pruritis is the most distressing symptom, which leads to wound excoriation and chronic wound formation. In spite of the clinical significance of abnormal innervation in scars, the nervous system has been largely ignored in the pathophysiology of hypertrophic scars. Evidence that neuropeptides contribute to inflammatory responses to injury include inflammatory cell chemotaxis, cytokine and growth factor production. The neuropeptide substance P, which is released from nerve endings after injury, induces inflammation and mediates angiogenesis, keratinocyte proliferation, and fibrogenesis. Substance P activity is tightly regulated by neutral endopeptidase (NEP), a membrane bound metallopeptidase that degrades substance P at the cell membrane. Altered substance P levels may contribute to impaired cutaneous healing responses associated with diabetes mellitus or hypertrophic scar formation. Topical application of exogenous substance P or an NEP inhibitor enhances wound closure kinetics in diabetic murine wounds suggesting that diabetic wounds have insufficient substance P levels to promote a neuroinflammatory response necessary for normal wound repair. Conversely, increased nerve numbers and neuropeptide levels with reduced NEP levels in human and porcine hypertrophic scar samples suggest that excessive neuropeptide activity induces exuberant inflammation in hypertrophic scars. Given these observations about the role of neuropeptides in cutaneous repair, neuronal modulation of repair processes at two extremes of abnormal wound healing, chronic non‐healing ulcers in type II diabetes mellitus and hypertrophic scars in deep partial thickness wounds, may provide therapeutic targets.</abstract><cop>Malden, USA</cop><pub>Blackwell Publishing Inc</pub><pmid>17727464</pmid><doi>10.1111/j.1524-475X.2007.00222.x</doi><tpages>5</tpages></addata></record> |
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subjects | Animals Burns - physiopathology Cicatrix, Hypertrophic - physiopathology Endopeptidases - physiology Humans Neuropeptides - blood Neuropeptides - physiology Peripheral Nerves - physiology Proprioception - physiology Protease Inhibitors - pharmacology Substance P - blood Substance P - physiology Wound Healing - physiology |
title | Making sense of hypertrophic scar: a role for nerves |
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