Nitric Oxide Synthase Gene Transfer Overcomes the Inhibition of Wound Healing by Sulfur Mustard in a Human Keratinocyte In Vitro Model
Sulfur mustard (SM) is a chemical warfare agent that causes extensive skin injury. Previously we reported that SM exposure resulted in suppression of inducible nitric oxide synthase (iNOS) expression to inhibit the healing of scratch wounds in a cultured normal human epidermal keratinocyte (NHEK) mo...
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Veröffentlicht in: | ISRN toxicology 2012, Vol.2012 (2012), p.1-9 |
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description | Sulfur mustard (SM) is a chemical warfare agent that causes extensive skin injury. Previously we reported that SM exposure resulted in suppression of inducible nitric oxide synthase (iNOS) expression to inhibit the healing of scratch wounds in a cultured normal human epidermal keratinocyte (NHEK) model. Based on this finding, the present study was to use adenovirus-mediated gene transfer of iNOS to restore the nitric oxide (NO) supply depleted by exposure to SM and to evaluate the effect of NO on wound healing inhibited by SM in NHEKs. The effect of the iNOS gene transfer on iNOS protein expression and NO generation were monitored by Western blot and flow cytometry, respectively. Wound healing with or without the iNOS gene transfer after SM exposure was assessed by light and confocal microscopy. The iNOS gene transfer via adenovirus resulted in overexpression of the iNOS and an increase in NO production regardless of SM exposure in the NHEK model. The gene transfer was also effective in overcoming the inhibition of wound healing due to SM exposure leading to the promotion of wound closure. The findings in this study suggest that the iNOS gene transfer is a promising therapeutic strategy for SM-induced skin injury. |
doi_str_mv | 10.5402/2012/190429 |
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I. ; Hakura, A. ; Borbély, G. ; Flora, S. J. S.</contributor><creatorcontrib>Ray, Prabhati ; Ishida, Keiko ; Amnuaysirikul, Jack ; Ishida, Hiroshi ; Ray, Radharaman ; Bannon, D. I. ; Hakura, A. ; Borbély, G. ; Flora, S. J. S.</creatorcontrib><description>Sulfur mustard (SM) is a chemical warfare agent that causes extensive skin injury. Previously we reported that SM exposure resulted in suppression of inducible nitric oxide synthase (iNOS) expression to inhibit the healing of scratch wounds in a cultured normal human epidermal keratinocyte (NHEK) model. Based on this finding, the present study was to use adenovirus-mediated gene transfer of iNOS to restore the nitric oxide (NO) supply depleted by exposure to SM and to evaluate the effect of NO on wound healing inhibited by SM in NHEKs. The effect of the iNOS gene transfer on iNOS protein expression and NO generation were monitored by Western blot and flow cytometry, respectively. Wound healing with or without the iNOS gene transfer after SM exposure was assessed by light and confocal microscopy. The iNOS gene transfer via adenovirus resulted in overexpression of the iNOS and an increase in NO production regardless of SM exposure in the NHEK model. The gene transfer was also effective in overcoming the inhibition of wound healing due to SM exposure leading to the promotion of wound closure. The findings in this study suggest that the iNOS gene transfer is a promising therapeutic strategy for SM-induced skin injury.</description><identifier>ISSN: 2090-6188</identifier><identifier>ISSN: 2090-6196</identifier><identifier>EISSN: 2090-6196</identifier><identifier>DOI: 10.5402/2012/190429</identifier><identifier>PMID: 23762631</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Puplishing Corporation</publisher><ispartof>ISRN toxicology, 2012, Vol.2012 (2012), p.1-9</ispartof><rights>Copyright © 2012 Hiroshi Ishida et al.</rights><rights>Copyright © 2012 Hiroshi Ishida et al. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2839-9283f66d12da28367f1b2f829b8cd16f6055061ef5fadc927a3bcf1591411e113</citedby><cites>FETCH-LOGICAL-c2839-9283f66d12da28367f1b2f829b8cd16f6055061ef5fadc927a3bcf1591411e113</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3664197/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3664197/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,4024,27923,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23762631$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Bannon, D. I.</contributor><contributor>Hakura, A.</contributor><contributor>Borbély, G.</contributor><contributor>Flora, S. J. S.</contributor><creatorcontrib>Ray, Prabhati</creatorcontrib><creatorcontrib>Ishida, Keiko</creatorcontrib><creatorcontrib>Amnuaysirikul, Jack</creatorcontrib><creatorcontrib>Ishida, Hiroshi</creatorcontrib><creatorcontrib>Ray, Radharaman</creatorcontrib><title>Nitric Oxide Synthase Gene Transfer Overcomes the Inhibition of Wound Healing by Sulfur Mustard in a Human Keratinocyte In Vitro Model</title><title>ISRN toxicology</title><addtitle>ISRN Toxicol</addtitle><description>Sulfur mustard (SM) is a chemical warfare agent that causes extensive skin injury. Previously we reported that SM exposure resulted in suppression of inducible nitric oxide synthase (iNOS) expression to inhibit the healing of scratch wounds in a cultured normal human epidermal keratinocyte (NHEK) model. Based on this finding, the present study was to use adenovirus-mediated gene transfer of iNOS to restore the nitric oxide (NO) supply depleted by exposure to SM and to evaluate the effect of NO on wound healing inhibited by SM in NHEKs. The effect of the iNOS gene transfer on iNOS protein expression and NO generation were monitored by Western blot and flow cytometry, respectively. Wound healing with or without the iNOS gene transfer after SM exposure was assessed by light and confocal microscopy. The iNOS gene transfer via adenovirus resulted in overexpression of the iNOS and an increase in NO production regardless of SM exposure in the NHEK model. The gene transfer was also effective in overcoming the inhibition of wound healing due to SM exposure leading to the promotion of wound closure. The findings in this study suggest that the iNOS gene transfer is a promising therapeutic strategy for SM-induced skin injury.</description><issn>2090-6188</issn><issn>2090-6196</issn><issn>2090-6196</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><recordid>eNqFkcFu1DAQhiMEolXpiTNozqClHjtx4gsSqqBb0bKHFjhGjj1ujLJ2ZSeFfQGem6wCKzjhw3ik-fyN5L8oniN7U5WMn3GG_AwVK7l6VBxzpthKopKPD33THBWnOX9j85G8rnjztDjiopZcCjwufn7yY_IGNj-8JbjZhbHXmeCCAsFt0iE7SrB5oGTiljKMPcFl6H3nRx8DRAdf4xQsrEkPPtxBt4ObaXBTguspjzpZ8AE0rKetDvCRkh59iGY37i3wZV4d4TpaGp4VT5weMp3-vk-Kzx_e356vV1ebi8vzd1crwxuhVmquTkqL3Oq5lbXDjruGq64xFqWTrKqYRHKV09YoXmvRGYeVwhKREMVJ8Xbx3k_dlqyhMCY9tPfJb3XatVH79t9J8H17Fx9aIWWJqp4FrxeBSTHnRO7wFlm7T6TdJ9Iuicz0y7_XHdg__z8Drxag98Hq7_4_thcLTDNCTh_gshJYCfELPjaeGA</recordid><startdate>2012</startdate><enddate>2012</enddate><creator>Ray, Prabhati</creator><creator>Ishida, Keiko</creator><creator>Amnuaysirikul, Jack</creator><creator>Ishida, Hiroshi</creator><creator>Ray, Radharaman</creator><general>Hindawi Puplishing Corporation</general><general>International Scholarly Research Network</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>5PM</scope></search><sort><creationdate>2012</creationdate><title>Nitric Oxide Synthase Gene Transfer Overcomes the Inhibition of Wound Healing by Sulfur Mustard in a Human Keratinocyte In Vitro Model</title><author>Ray, Prabhati ; Ishida, Keiko ; Amnuaysirikul, Jack ; Ishida, Hiroshi ; Ray, Radharaman</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2839-9283f66d12da28367f1b2f829b8cd16f6055061ef5fadc927a3bcf1591411e113</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ray, Prabhati</creatorcontrib><creatorcontrib>Ishida, Keiko</creatorcontrib><creatorcontrib>Amnuaysirikul, Jack</creatorcontrib><creatorcontrib>Ishida, Hiroshi</creatorcontrib><creatorcontrib>Ray, Radharaman</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>ISRN toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ray, Prabhati</au><au>Ishida, Keiko</au><au>Amnuaysirikul, Jack</au><au>Ishida, Hiroshi</au><au>Ray, Radharaman</au><au>Bannon, D. I.</au><au>Hakura, A.</au><au>Borbély, G.</au><au>Flora, S. J. S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nitric Oxide Synthase Gene Transfer Overcomes the Inhibition of Wound Healing by Sulfur Mustard in a Human Keratinocyte In Vitro Model</atitle><jtitle>ISRN toxicology</jtitle><addtitle>ISRN Toxicol</addtitle><date>2012</date><risdate>2012</risdate><volume>2012</volume><issue>2012</issue><spage>1</spage><epage>9</epage><pages>1-9</pages><issn>2090-6188</issn><issn>2090-6196</issn><eissn>2090-6196</eissn><abstract>Sulfur mustard (SM) is a chemical warfare agent that causes extensive skin injury. Previously we reported that SM exposure resulted in suppression of inducible nitric oxide synthase (iNOS) expression to inhibit the healing of scratch wounds in a cultured normal human epidermal keratinocyte (NHEK) model. Based on this finding, the present study was to use adenovirus-mediated gene transfer of iNOS to restore the nitric oxide (NO) supply depleted by exposure to SM and to evaluate the effect of NO on wound healing inhibited by SM in NHEKs. The effect of the iNOS gene transfer on iNOS protein expression and NO generation were monitored by Western blot and flow cytometry, respectively. Wound healing with or without the iNOS gene transfer after SM exposure was assessed by light and confocal microscopy. The iNOS gene transfer via adenovirus resulted in overexpression of the iNOS and an increase in NO production regardless of SM exposure in the NHEK model. The gene transfer was also effective in overcoming the inhibition of wound healing due to SM exposure leading to the promotion of wound closure. The findings in this study suggest that the iNOS gene transfer is a promising therapeutic strategy for SM-induced skin injury.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Puplishing Corporation</pub><pmid>23762631</pmid><doi>10.5402/2012/190429</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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title | Nitric Oxide Synthase Gene Transfer Overcomes the Inhibition of Wound Healing by Sulfur Mustard in a Human Keratinocyte In Vitro Model |
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