TLR2 expression and signaling-dependent inflammation impair wound healing in diabetic mice
Toll-like receptor-2 (TLR2) is a pivotal pathogen recognition receptor that has a key role in inflammation, diabetes, and injury. Hyperglycemia, inflammation, and oxidative stress induce TLR2-myeloid differentiation factor-88 (MyD88) expression and signaling, and are major pathophysiological mechani...
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| Veröffentlicht in: | Laboratory investigation 2010-11, Vol.90 (11), p.1628-1636 |
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| creator | Dasu, Mohan R Thangappan, Ravi K Bourgette, Alika DiPietro, Luisa A Isseroff, Rivkah Jialal, Ishwarlal |
| description | Toll-like receptor-2 (TLR2) is a pivotal pathogen recognition receptor that has a key role in inflammation, diabetes, and injury. Hyperglycemia, inflammation, and oxidative stress induce TLR2-myeloid differentiation factor-88 (MyD88) expression and signaling, and are major pathophysiological mechanisms in the impaired diabetic wound-healing process. The aim of the study was to examine the contribution of TLR2-MyD88 expression and signaling to the prolonged inflammation observed in diabetic wounds. Diabetes was induced in male C57BL/6J and TLR2−/− mice using streptozotocin (STZ) with matching nondiabetic mice as control. In addition, nonobese diabetic (NOD) mice were used to represent the spontaneous type 1 diabetes condition. After 2 weeks of persistent hyperglycemia in the mice, full-thickness excision wounds were made on the backs aseptically. Total RNA and protein were subjected to real-time PCR and western blot analyses. Wound sizes were measured using digital planimetry. TLR2 mRNA and protein expression increased significantly in wounds of C57BL/6J+STZ and NOD mice (P |
| doi_str_mv | 10.1038/labinvest.2010.158 |
| format | Article |
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Hyperglycemia, inflammation, and oxidative stress induce TLR2-myeloid differentiation factor-88 (MyD88) expression and signaling, and are major pathophysiological mechanisms in the impaired diabetic wound-healing process. The aim of the study was to examine the contribution of TLR2-MyD88 expression and signaling to the prolonged inflammation observed in diabetic wounds. Diabetes was induced in male C57BL/6J and TLR2−/− mice using streptozotocin (STZ) with matching nondiabetic mice as control. In addition, nonobese diabetic (NOD) mice were used to represent the spontaneous type 1 diabetes condition. After 2 weeks of persistent hyperglycemia in the mice, full-thickness excision wounds were made on the backs aseptically. Total RNA and protein were subjected to real-time PCR and western blot analyses. Wound sizes were measured using digital planimetry. TLR2 mRNA and protein expression increased significantly in wounds of C57BL/6J+STZ and NOD mice (P<0.05) compared with nondiabetic C57BL/6J mice. MyD88 expression, interleukin receptor-associated kinase-1 phosphorylation, and nuclear factor-κ B (NF-κB) activation were increased in diabetic wounds compared with nondiabetic wounds. Wounds of TLR2−/−+STZ mice showed less oxidative stress, decreased MyD88 signaling, NF-κB activation, and cytokine secretion. The wound closure was significant in TLR2−/−+ STZ mice compared with C57BL/6J+STZ mice. Collectively, our findings show that increased TLR2 mRNA and protein expression, signaling, and activation contribute to the prolonged inflammation in the diabetic wounds and that absence of TLR2 may result in decreased inflammation and improved wound healing.</description><identifier>ISSN: 0023-6837</identifier><identifier>EISSN: 1530-0307</identifier><identifier>DOI: 10.1038/labinvest.2010.158</identifier><identifier>PMID: 20733560</identifier><identifier>CODEN: LAINAW</identifier><language>eng</language><publisher>New York: Elsevier Inc</publisher><subject>631/208/199 ; 631/250/256 ; 631/250/262/2106/2108 ; 692/699/2743/137/1418 ; Animals ; Biological and medical sciences ; Biotechnology ; cytokines ; Diabetes Mellitus, Experimental - physiopathology ; Fundamental and applied biological sciences. Psychology ; inflammation ; Inflammation - physiopathology ; Investigative techniques, diagnostic techniques (general aspects) ; Laboratory Medicine ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Mice ; Mice, Inbred C57BL ; Myeloid Differentiation Factor 88 - physiology ; NF-κB ; Pathology ; research-article ; Signal Transduction - physiology ; Streptozocin ; Toll-like receptor 2 ; Toll-Like Receptor 2 - physiology ; type 1 diabetes ; Wound Healing</subject><ispartof>Laboratory investigation, 2010-11, Vol.90 (11), p.1628-1636</ispartof><rights>2010 United States & Canadian Academy of Pathology</rights><rights>United States and Canadian Academy of Pathology, Inc. 2010</rights><rights>2015 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Nov 2010</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c585t-19c2bc9991dd17a109c25edc2b91e4023d81ffc956698f14b800630d033bb3483</citedby><cites>FETCH-LOGICAL-c585t-19c2bc9991dd17a109c25edc2b91e4023d81ffc956698f14b800630d033bb3483</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27906,27907</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23531342$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20733560$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dasu, Mohan R</creatorcontrib><creatorcontrib>Thangappan, Ravi K</creatorcontrib><creatorcontrib>Bourgette, Alika</creatorcontrib><creatorcontrib>DiPietro, Luisa A</creatorcontrib><creatorcontrib>Isseroff, Rivkah</creatorcontrib><creatorcontrib>Jialal, Ishwarlal</creatorcontrib><title>TLR2 expression and signaling-dependent inflammation impair wound healing in diabetic mice</title><title>Laboratory investigation</title><addtitle>Lab Invest</addtitle><addtitle>Lab Invest</addtitle><description>Toll-like receptor-2 (TLR2) is a pivotal pathogen recognition receptor that has a key role in inflammation, diabetes, and injury. Hyperglycemia, inflammation, and oxidative stress induce TLR2-myeloid differentiation factor-88 (MyD88) expression and signaling, and are major pathophysiological mechanisms in the impaired diabetic wound-healing process. The aim of the study was to examine the contribution of TLR2-MyD88 expression and signaling to the prolonged inflammation observed in diabetic wounds. Diabetes was induced in male C57BL/6J and TLR2−/− mice using streptozotocin (STZ) with matching nondiabetic mice as control. In addition, nonobese diabetic (NOD) mice were used to represent the spontaneous type 1 diabetes condition. After 2 weeks of persistent hyperglycemia in the mice, full-thickness excision wounds were made on the backs aseptically. Total RNA and protein were subjected to real-time PCR and western blot analyses. Wound sizes were measured using digital planimetry. TLR2 mRNA and protein expression increased significantly in wounds of C57BL/6J+STZ and NOD mice (P<0.05) compared with nondiabetic C57BL/6J mice. MyD88 expression, interleukin receptor-associated kinase-1 phosphorylation, and nuclear factor-κ B (NF-κB) activation were increased in diabetic wounds compared with nondiabetic wounds. Wounds of TLR2−/−+STZ mice showed less oxidative stress, decreased MyD88 signaling, NF-κB activation, and cytokine secretion. The wound closure was significant in TLR2−/−+ STZ mice compared with C57BL/6J+STZ mice. Collectively, our findings show that increased TLR2 mRNA and protein expression, signaling, and activation contribute to the prolonged inflammation in the diabetic wounds and that absence of TLR2 may result in decreased inflammation and improved wound healing.</description><subject>631/208/199</subject><subject>631/250/256</subject><subject>631/250/262/2106/2108</subject><subject>692/699/2743/137/1418</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Biotechnology</subject><subject>cytokines</subject><subject>Diabetes Mellitus, Experimental - physiopathology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>inflammation</subject><subject>Inflammation - physiopathology</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Laboratory Medicine</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Myeloid Differentiation Factor 88 - physiology</subject><subject>NF-κB</subject><subject>Pathology</subject><subject>research-article</subject><subject>Signal Transduction - physiology</subject><subject>Streptozocin</subject><subject>Toll-like receptor 2</subject><subject>Toll-Like Receptor 2 - physiology</subject><subject>type 1 diabetes</subject><subject>Wound Healing</subject><issn>0023-6837</issn><issn>1530-0307</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqF0U1v1DAQBmALUdGl8Ac4oAgJOKWM7Xw4Ui-oKlBppUqoXLhYjj1ZXCVOsJNC_z02WbYSh_YUxXlmxpmXkFcUTilw8aFXrXW3GOZTBumsFE_IhpYccuBQPyUbAMbzSvD6mDwP4QaAFkVVPiPHDGrOywo25Pv19ivL8PfkMQQ7ukw5kwW7c6q3bpcbnNAZdHNmXderYVBzQnaYlPXZr3GJ-gf-tVFkxqoWZ6uzwWp8QY461Qd8uX-ekG-fLq7Pv-Tbq8-X5x-3uS5FOee00azVTdNQY2itKMT3Ek08bCgW8Q-MoF2nm7KqGtHRohUAFQcDnLctLwQ_Ie_XvpMffy5xHXKwQWPfK4fjEmQDdVpKTR-VdcWKmhYsyTf_yZtx8XEpCVEqgFZpMFuR9mMIHjs5eTsofycpyJSQPCQkU0IyJhSLXu87L-2A5lDyL5II3u6BClr1nVdO23DveMkpL1h0fHUhfnI79PdXfHD8u7XKqXnxeGh7oEmu8GyFGKO7tbF90BadRmM96lma0T405w_hQM5G</recordid><startdate>20101101</startdate><enddate>20101101</enddate><creator>Dasu, Mohan R</creator><creator>Thangappan, Ravi K</creator><creator>Bourgette, Alika</creator><creator>DiPietro, Luisa A</creator><creator>Isseroff, Rivkah</creator><creator>Jialal, Ishwarlal</creator><general>Elsevier Inc</general><general>Nature Publishing Group US</general><general>Nature Publishing Group</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</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>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20101101</creationdate><title>TLR2 expression and signaling-dependent inflammation impair wound healing in diabetic mice</title><author>Dasu, Mohan R ; Thangappan, Ravi K ; Bourgette, Alika ; DiPietro, Luisa A ; Isseroff, Rivkah ; Jialal, Ishwarlal</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c585t-19c2bc9991dd17a109c25edc2b91e4023d81ffc956698f14b800630d033bb3483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>631/208/199</topic><topic>631/250/256</topic><topic>631/250/262/2106/2108</topic><topic>692/699/2743/137/1418</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Biotechnology</topic><topic>cytokines</topic><topic>Diabetes Mellitus, Experimental - physiopathology</topic><topic>Fundamental and applied biological sciences. 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Academic</collection><jtitle>Laboratory investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dasu, Mohan R</au><au>Thangappan, Ravi K</au><au>Bourgette, Alika</au><au>DiPietro, Luisa A</au><au>Isseroff, Rivkah</au><au>Jialal, Ishwarlal</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TLR2 expression and signaling-dependent inflammation impair wound healing in diabetic mice</atitle><jtitle>Laboratory investigation</jtitle><stitle>Lab Invest</stitle><addtitle>Lab Invest</addtitle><date>2010-11-01</date><risdate>2010</risdate><volume>90</volume><issue>11</issue><spage>1628</spage><epage>1636</epage><pages>1628-1636</pages><issn>0023-6837</issn><eissn>1530-0307</eissn><coden>LAINAW</coden><abstract>Toll-like receptor-2 (TLR2) is a pivotal pathogen recognition receptor that has a key role in inflammation, diabetes, and injury. Hyperglycemia, inflammation, and oxidative stress induce TLR2-myeloid differentiation factor-88 (MyD88) expression and signaling, and are major pathophysiological mechanisms in the impaired diabetic wound-healing process. The aim of the study was to examine the contribution of TLR2-MyD88 expression and signaling to the prolonged inflammation observed in diabetic wounds. Diabetes was induced in male C57BL/6J and TLR2−/− mice using streptozotocin (STZ) with matching nondiabetic mice as control. In addition, nonobese diabetic (NOD) mice were used to represent the spontaneous type 1 diabetes condition. After 2 weeks of persistent hyperglycemia in the mice, full-thickness excision wounds were made on the backs aseptically. Total RNA and protein were subjected to real-time PCR and western blot analyses. Wound sizes were measured using digital planimetry. TLR2 mRNA and protein expression increased significantly in wounds of C57BL/6J+STZ and NOD mice (P<0.05) compared with nondiabetic C57BL/6J mice. MyD88 expression, interleukin receptor-associated kinase-1 phosphorylation, and nuclear factor-κ B (NF-κB) activation were increased in diabetic wounds compared with nondiabetic wounds. Wounds of TLR2−/−+STZ mice showed less oxidative stress, decreased MyD88 signaling, NF-κB activation, and cytokine secretion. The wound closure was significant in TLR2−/−+ STZ mice compared with C57BL/6J+STZ mice. Collectively, our findings show that increased TLR2 mRNA and protein expression, signaling, and activation contribute to the prolonged inflammation in the diabetic wounds and that absence of TLR2 may result in decreased inflammation and improved wound healing.</abstract><cop>New York</cop><pub>Elsevier Inc</pub><pmid>20733560</pmid><doi>10.1038/labinvest.2010.158</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 631/208/199 631/250/256 631/250/262/2106/2108 692/699/2743/137/1418 Animals Biological and medical sciences Biotechnology cytokines Diabetes Mellitus, Experimental - physiopathology Fundamental and applied biological sciences. Psychology inflammation Inflammation - physiopathology Investigative techniques, diagnostic techniques (general aspects) Laboratory Medicine Male Medical sciences Medicine Medicine & Public Health Mice Mice, Inbred C57BL Myeloid Differentiation Factor 88 - physiology NF-κB Pathology research-article Signal Transduction - physiology Streptozocin Toll-like receptor 2 Toll-Like Receptor 2 - physiology type 1 diabetes Wound Healing |
| title | TLR2 expression and signaling-dependent inflammation impair wound healing in diabetic mice |
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