Granulocyte-macrophage colony-stimulating factor enhances wound healing in diabetes via upregulation of proinflammatory cytokines
Summary Background Chronic ulceration, especially in diabetes, remains a substantial clinical problem. Exogenous granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) is efficacious in the treatment of chronic wound healing in both animal models and patients, but its role in diabetic wounds rem...
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Veröffentlicht in: | British journal of dermatology (1951) 2010-03, Vol.162 (3), p.478-486 |
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creator | Fang, Y. Shen, J. Yao, M. Beagley, K.W. Hambly, B.D. Bao, S. |
description | Summary Background Chronic ulceration, especially in diabetes, remains a substantial clinical problem. Exogenous granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) is efficacious in the treatment of chronic wound healing in both animal models and patients, but its role in diabetic wounds remains to be explored.
Objectives Using a diabetic mouse model, to investigate the role of GM‐CSF in wound healing.
Methods Clinical observation, histopathology, immunohistochemistry and cytokine assays.
Results There was a significant reduction (50%) in GM‐CSF production in the wounds of the diabetics compared with nondiabetics. Exogenous GM‐CSF substantially enhanced the wound healing in diabetic mice, accompanied by increased interleukin‐6 and monocyte chemoattractant protein‐1 production. The elevated cytokines correlated with increased neovascularization, and infiltration of macrophages and neutrophils. GM‐CSF showed no beneficial effects in nondiabetic wound healing.
Conclusions Our results provide useful guidelines for the clinical management of chronic ulceration in diabetes. |
doi_str_mv | 10.1111/j.1365-2133.2009.09528.x |
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Objectives Using a diabetic mouse model, to investigate the role of GM‐CSF in wound healing.
Methods Clinical observation, histopathology, immunohistochemistry and cytokine assays.
Results There was a significant reduction (50%) in GM‐CSF production in the wounds of the diabetics compared with nondiabetics. Exogenous GM‐CSF substantially enhanced the wound healing in diabetic mice, accompanied by increased interleukin‐6 and monocyte chemoattractant protein‐1 production. The elevated cytokines correlated with increased neovascularization, and infiltration of macrophages and neutrophils. GM‐CSF showed no beneficial effects in nondiabetic wound healing.
Conclusions Our results provide useful guidelines for the clinical management of chronic ulceration in diabetes.</description><identifier>ISSN: 0007-0963</identifier><identifier>EISSN: 1365-2133</identifier><identifier>DOI: 10.1111/j.1365-2133.2009.09528.x</identifier><identifier>PMID: 19799605</identifier><identifier>CODEN: BJDEAZ</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Analysis of Variance ; Animals ; Biological and medical sciences ; Chemokine CCL2 - biosynthesis ; Collagen - metabolism ; Colony-Stimulating Factors - metabolism ; cytokines ; Cytokines - metabolism ; Dermatology ; diabetes ; Diabetes Mellitus, Experimental - metabolism ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; granulocyte-macrophage colony-stimulating factor ; Granulocyte-Macrophage Colony-Stimulating Factor - metabolism ; Interleukin-6 - biosynthesis ; Male ; Medical sciences ; Mice ; Mice, Knockout ; Models, Animal ; Neovascularization, Physiologic - physiology ; proinflammatory wound healing ; Up-Regulation - physiology ; Wound Healing - physiology</subject><ispartof>British journal of dermatology (1951), 2010-03, Vol.162 (3), p.478-486</ispartof><rights>2009 The Authors. Journal Compilation © 2009 British Association of Dermatologists</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4848-74be871fa6ef22e04ed137fce347a69670931ffe05dbbdc6617a5e1a9e0c30fb3</citedby></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.1365-2133.2009.09528.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1365-2133.2009.09528.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22506055$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19799605$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fang, Y.</creatorcontrib><creatorcontrib>Shen, J.</creatorcontrib><creatorcontrib>Yao, M.</creatorcontrib><creatorcontrib>Beagley, K.W.</creatorcontrib><creatorcontrib>Hambly, B.D.</creatorcontrib><creatorcontrib>Bao, S.</creatorcontrib><title>Granulocyte-macrophage colony-stimulating factor enhances wound healing in diabetes via upregulation of proinflammatory cytokines</title><title>British journal of dermatology (1951)</title><addtitle>Br J Dermatol</addtitle><description>Summary Background Chronic ulceration, especially in diabetes, remains a substantial clinical problem. Exogenous granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) is efficacious in the treatment of chronic wound healing in both animal models and patients, but its role in diabetic wounds remains to be explored.
Objectives Using a diabetic mouse model, to investigate the role of GM‐CSF in wound healing.
Methods Clinical observation, histopathology, immunohistochemistry and cytokine assays.
Results There was a significant reduction (50%) in GM‐CSF production in the wounds of the diabetics compared with nondiabetics. Exogenous GM‐CSF substantially enhanced the wound healing in diabetic mice, accompanied by increased interleukin‐6 and monocyte chemoattractant protein‐1 production. The elevated cytokines correlated with increased neovascularization, and infiltration of macrophages and neutrophils. GM‐CSF showed no beneficial effects in nondiabetic wound healing.
Conclusions Our results provide useful guidelines for the clinical management of chronic ulceration in diabetes.</description><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Chemokine CCL2 - biosynthesis</subject><subject>Collagen - metabolism</subject><subject>Colony-Stimulating Factors - metabolism</subject><subject>cytokines</subject><subject>Cytokines - metabolism</subject><subject>Dermatology</subject><subject>diabetes</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>granulocyte-macrophage colony-stimulating factor</subject><subject>Granulocyte-Macrophage Colony-Stimulating Factor - metabolism</subject><subject>Interleukin-6 - biosynthesis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Models, Animal</subject><subject>Neovascularization, Physiologic - physiology</subject><subject>proinflammatory wound healing</subject><subject>Up-Regulation - physiology</subject><subject>Wound Healing - physiology</subject><issn>0007-0963</issn><issn>1365-2133</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU-P0zAQxSMEYsvCV0C-AKcEO07s5MCBXaCAViAt_47WxBm37iZ2iRO2PfLNcbal3PDFlub3ZjzvJQlhNGPxvNxkjIsyzRnnWU5pndG6zKtsdy9ZnAr3kwWlVKa0FvwseRTChlLGaUkfJmeslnUtaLlIfi8HcFPn9X7EtAc9-O0aVki077zbp2G0_dTBaN2KGNCjHwi6NTiNgdz6ybVkjdDNVetIa6HBMVZ-WSDTdsDVndQ74g3ZDt4600HfQ-yyJ3Ggv7EOw-PkgYEu4JPjfZ58e_f26-X79Orz8sPl66tUF1VRpbJosJLMgECT50gLbBmXRiMvJIhaSFpzZgzSsm2aVgvBJJTIoEaqOTUNP09eHPrGn_ycMIyqt0Fj14FDPwUlOa9EIYSM5PP_kjkro-dFFcGnR3BqemzVdrA9DHv1194IPDsCEDR0JnqtbThxeV7SiM3cqwN3azvc_-tD1Ry32qg5VTWnqua41V3caqcuPr6ZX1GfHvQ2jLg76WG4UXEfWaofn5Yq7vb9-uJLra75H6QUsE8</recordid><startdate>201003</startdate><enddate>201003</enddate><creator>Fang, Y.</creator><creator>Shen, J.</creator><creator>Yao, M.</creator><creator>Beagley, K.W.</creator><creator>Hambly, B.D.</creator><creator>Bao, S.</creator><general>Blackwell Publishing Ltd</general><general>Wiley-Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>201003</creationdate><title>Granulocyte-macrophage colony-stimulating factor enhances wound healing in diabetes via upregulation of proinflammatory cytokines</title><author>Fang, Y. ; Shen, J. ; Yao, M. ; Beagley, K.W. ; Hambly, B.D. ; Bao, S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4848-74be871fa6ef22e04ed137fce347a69670931ffe05dbbdc6617a5e1a9e0c30fb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Chemokine CCL2 - biosynthesis</topic><topic>Collagen - metabolism</topic><topic>Colony-Stimulating Factors - metabolism</topic><topic>cytokines</topic><topic>Cytokines - metabolism</topic><topic>Dermatology</topic><topic>diabetes</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Female</topic><topic>granulocyte-macrophage colony-stimulating factor</topic><topic>Granulocyte-Macrophage Colony-Stimulating Factor - metabolism</topic><topic>Interleukin-6 - biosynthesis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Models, Animal</topic><topic>Neovascularization, Physiologic - physiology</topic><topic>proinflammatory wound healing</topic><topic>Up-Regulation - physiology</topic><topic>Wound Healing - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fang, Y.</creatorcontrib><creatorcontrib>Shen, J.</creatorcontrib><creatorcontrib>Yao, M.</creatorcontrib><creatorcontrib>Beagley, K.W.</creatorcontrib><creatorcontrib>Hambly, B.D.</creatorcontrib><creatorcontrib>Bao, S.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>British journal of dermatology (1951)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fang, Y.</au><au>Shen, J.</au><au>Yao, M.</au><au>Beagley, K.W.</au><au>Hambly, B.D.</au><au>Bao, S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Granulocyte-macrophage colony-stimulating factor enhances wound healing in diabetes via upregulation of proinflammatory cytokines</atitle><jtitle>British journal of dermatology (1951)</jtitle><addtitle>Br J Dermatol</addtitle><date>2010-03</date><risdate>2010</risdate><volume>162</volume><issue>3</issue><spage>478</spage><epage>486</epage><pages>478-486</pages><issn>0007-0963</issn><eissn>1365-2133</eissn><coden>BJDEAZ</coden><abstract>Summary Background Chronic ulceration, especially in diabetes, remains a substantial clinical problem. Exogenous granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) is efficacious in the treatment of chronic wound healing in both animal models and patients, but its role in diabetic wounds remains to be explored.
Objectives Using a diabetic mouse model, to investigate the role of GM‐CSF in wound healing.
Methods Clinical observation, histopathology, immunohistochemistry and cytokine assays.
Results There was a significant reduction (50%) in GM‐CSF production in the wounds of the diabetics compared with nondiabetics. Exogenous GM‐CSF substantially enhanced the wound healing in diabetic mice, accompanied by increased interleukin‐6 and monocyte chemoattractant protein‐1 production. The elevated cytokines correlated with increased neovascularization, and infiltration of macrophages and neutrophils. GM‐CSF showed no beneficial effects in nondiabetic wound healing.
Conclusions Our results provide useful guidelines for the clinical management of chronic ulceration in diabetes.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>19799605</pmid><doi>10.1111/j.1365-2133.2009.09528.x</doi><tpages>9</tpages></addata></record> |
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subjects | Analysis of Variance Animals Biological and medical sciences Chemokine CCL2 - biosynthesis Collagen - metabolism Colony-Stimulating Factors - metabolism cytokines Cytokines - metabolism Dermatology diabetes Diabetes Mellitus, Experimental - metabolism Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female granulocyte-macrophage colony-stimulating factor Granulocyte-Macrophage Colony-Stimulating Factor - metabolism Interleukin-6 - biosynthesis Male Medical sciences Mice Mice, Knockout Models, Animal Neovascularization, Physiologic - physiology proinflammatory wound healing Up-Regulation - physiology Wound Healing - physiology |
title | Granulocyte-macrophage colony-stimulating factor enhances wound healing in diabetes via upregulation of proinflammatory cytokines |
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