Inhibition of skin fibrosis in systemic sclerosis by botulinum toxin B via the suppression of oxidative stress
Oxidative stress has been reported to play an important role in the pathogenesis of skin fibrosis in systemic sclerosis (SSc). We previously identified that botulinum toxin (BTX) injection suppresses pressure ulcer formation in a cutaneous ischemia–reperfusion injury mouse model by regulation of oxi...
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| Veröffentlicht in: | Journal of dermatology 2021-07, Vol.48 (7), p.1052-1061 |
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| creator | Baral, Hritu Sekiguchi, Akiko Uchiyama, Akihiko Nisaa Amalia, Syahla Yamazaki, Sahori Inoue, Yuta Yokoyama, Yoko Ogino, Sachiko Torii, Ryoko Hosoi, Mari Akai, Ryoko Iwawaki, Takao Ishikawa, Osamu Motegi, Sei‐ichiro |
| description | Oxidative stress has been reported to play an important role in the pathogenesis of skin fibrosis in systemic sclerosis (SSc). We previously identified that botulinum toxin (BTX) injection suppresses pressure ulcer formation in a cutaneous ischemia–reperfusion injury mouse model by regulation of oxidative stress. However, the therapeutic possibility of BTX administration for preventing skin fibrosis in SSc is unclear. The objective of this study was to investigate the effect of BTX‐B on skin fibrosis in a murine model of SSc and determine the underlying mechanism. We found that BTX‐B injection significantly reduced dermal thickness and inflammatory cell infiltration in bleomycin‐induced skin fibrosis lesion in mice. We also identified that the oxidative stress signal detected through bioluminescence in OKD48 mice after bleomycin injection in the skin was significantly decreased by BTX‐B. Additionally, mRNA levels of oxidative stress associated factors (NOX2, HO‐1, Trx2) were significantly decreased by BTX‐B. Apoptotic cells in the lesional skin of bleomycin‐treated mice were significantly reduced by BTX‐B. Oxidant‐induced intracellular accumulation of reactive oxygen species in SSc fibroblasts was also inhibited by BTX‐B. In conclusion, BTX‐B might improve bleomycin‐induced skin fibrosis via the suppression of oxidative stress and inflammatory cells in the skin. BTX‐B injection may have a therapeutic effect on skin fibrosis in SSc. |
| doi_str_mv | 10.1111/1346-8138.15888 |
| format | Article |
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We previously identified that botulinum toxin (BTX) injection suppresses pressure ulcer formation in a cutaneous ischemia–reperfusion injury mouse model by regulation of oxidative stress. However, the therapeutic possibility of BTX administration for preventing skin fibrosis in SSc is unclear. The objective of this study was to investigate the effect of BTX‐B on skin fibrosis in a murine model of SSc and determine the underlying mechanism. We found that BTX‐B injection significantly reduced dermal thickness and inflammatory cell infiltration in bleomycin‐induced skin fibrosis lesion in mice. We also identified that the oxidative stress signal detected through bioluminescence in OKD48 mice after bleomycin injection in the skin was significantly decreased by BTX‐B. Additionally, mRNA levels of oxidative stress associated factors (NOX2, HO‐1, Trx2) were significantly decreased by BTX‐B. Apoptotic cells in the lesional skin of bleomycin‐treated mice were significantly reduced by BTX‐B. Oxidant‐induced intracellular accumulation of reactive oxygen species in SSc fibroblasts was also inhibited by BTX‐B. In conclusion, BTX‐B might improve bleomycin‐induced skin fibrosis via the suppression of oxidative stress and inflammatory cells in the skin. BTX‐B injection may have a therapeutic effect on skin fibrosis in SSc.</description><identifier>ISSN: 0385-2407</identifier><identifier>EISSN: 1346-8138</identifier><identifier>DOI: 10.1111/1346-8138.15888</identifier><identifier>PMID: 33840125</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Animal models ; Apoptosis ; Bioluminescence ; Bleomycin ; Botulinum toxin ; Botulinum toxin type B ; CYBB protein ; fibroblast ; Fibroblasts ; Fibrosis ; Inflammation ; Injection ; Injury prevention ; Ischemia ; mRNA ; Oxidants ; Oxidative stress ; Reactive oxygen species ; Reperfusion ; Scars ; Scleroderma ; Skin diseases ; skin fibrosis ; Systemic sclerosis</subject><ispartof>Journal of dermatology, 2021-07, Vol.48 (7), p.1052-1061</ispartof><rights>2021 Japanese Dermatological Association</rights><rights>2021 Japanese Dermatological Association.</rights><rights>Copyright © 2021 Japanese Dermatological Association</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4618-61b057bddd157095965ee290438ae57910ec35add3fa04933f144bba43b7d9dc3</citedby><cites>FETCH-LOGICAL-c4618-61b057bddd157095965ee290438ae57910ec35add3fa04933f144bba43b7d9dc3</cites><orcidid>0000-0002-2169-2427 ; 0000-0002-7016-337X ; 0000-0001-8286-0669</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2F1346-8138.15888$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2F1346-8138.15888$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33840125$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Baral, Hritu</creatorcontrib><creatorcontrib>Sekiguchi, Akiko</creatorcontrib><creatorcontrib>Uchiyama, Akihiko</creatorcontrib><creatorcontrib>Nisaa Amalia, Syahla</creatorcontrib><creatorcontrib>Yamazaki, Sahori</creatorcontrib><creatorcontrib>Inoue, Yuta</creatorcontrib><creatorcontrib>Yokoyama, Yoko</creatorcontrib><creatorcontrib>Ogino, Sachiko</creatorcontrib><creatorcontrib>Torii, Ryoko</creatorcontrib><creatorcontrib>Hosoi, Mari</creatorcontrib><creatorcontrib>Akai, Ryoko</creatorcontrib><creatorcontrib>Iwawaki, Takao</creatorcontrib><creatorcontrib>Ishikawa, Osamu</creatorcontrib><creatorcontrib>Motegi, Sei‐ichiro</creatorcontrib><title>Inhibition of skin fibrosis in systemic sclerosis by botulinum toxin B via the suppression of oxidative stress</title><title>Journal of dermatology</title><addtitle>J Dermatol</addtitle><description>Oxidative stress has been reported to play an important role in the pathogenesis of skin fibrosis in systemic sclerosis (SSc). We previously identified that botulinum toxin (BTX) injection suppresses pressure ulcer formation in a cutaneous ischemia–reperfusion injury mouse model by regulation of oxidative stress. However, the therapeutic possibility of BTX administration for preventing skin fibrosis in SSc is unclear. The objective of this study was to investigate the effect of BTX‐B on skin fibrosis in a murine model of SSc and determine the underlying mechanism. We found that BTX‐B injection significantly reduced dermal thickness and inflammatory cell infiltration in bleomycin‐induced skin fibrosis lesion in mice. We also identified that the oxidative stress signal detected through bioluminescence in OKD48 mice after bleomycin injection in the skin was significantly decreased by BTX‐B. Additionally, mRNA levels of oxidative stress associated factors (NOX2, HO‐1, Trx2) were significantly decreased by BTX‐B. Apoptotic cells in the lesional skin of bleomycin‐treated mice were significantly reduced by BTX‐B. Oxidant‐induced intracellular accumulation of reactive oxygen species in SSc fibroblasts was also inhibited by BTX‐B. In conclusion, BTX‐B might improve bleomycin‐induced skin fibrosis via the suppression of oxidative stress and inflammatory cells in the skin. BTX‐B injection may have a therapeutic effect on skin fibrosis in SSc.</description><subject>Animal models</subject><subject>Apoptosis</subject><subject>Bioluminescence</subject><subject>Bleomycin</subject><subject>Botulinum toxin</subject><subject>Botulinum toxin type B</subject><subject>CYBB protein</subject><subject>fibroblast</subject><subject>Fibroblasts</subject><subject>Fibrosis</subject><subject>Inflammation</subject><subject>Injection</subject><subject>Injury prevention</subject><subject>Ischemia</subject><subject>mRNA</subject><subject>Oxidants</subject><subject>Oxidative stress</subject><subject>Reactive oxygen species</subject><subject>Reperfusion</subject><subject>Scars</subject><subject>Scleroderma</subject><subject>Skin diseases</subject><subject>skin fibrosis</subject><subject>Systemic sclerosis</subject><issn>0385-2407</issn><issn>1346-8138</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNqFkb1PwzAQxS0EoqUwsyFLLCxp7dhO7BFKgaJKLDBbduyoLvkocVLof49LSgcWvJz17ndPp3cAXGI0xuFNMKFJxDHhY8w450dgeFCOwRARzqKYonQAzrxfIRQLhtEpGBDCKcIxG4JqXi2ddq2rK1jn0L-7CuZON7V3Hoa_3_rWli6DPitsr-ot1HXbFa7qStjWX4G6gxunYLu00HfrdWO93_uFrlGt24RGu5PPwUmuCm8v9nUE3h5mr9OnaPHyOJ_eLqKMJphHCdaIpdoYg1mKBBMJszYWiBKuLEsFRjYjTBlDcoWoICTHlGqtKNGpESYjI3DT-66b-qOzvpWl85ktClXZuvMyZhhzIRLOA3r9B13VXVOF7QJFEx7jWKSBmvRUFkLwjc3lunGlarYSI7k7hdwFL3fBy59ThImrvW-nS2sO_G_2AWA98OkKu_3PTz7fz3rjb4ygk88</recordid><startdate>202107</startdate><enddate>202107</enddate><creator>Baral, Hritu</creator><creator>Sekiguchi, Akiko</creator><creator>Uchiyama, Akihiko</creator><creator>Nisaa Amalia, Syahla</creator><creator>Yamazaki, Sahori</creator><creator>Inoue, Yuta</creator><creator>Yokoyama, Yoko</creator><creator>Ogino, Sachiko</creator><creator>Torii, Ryoko</creator><creator>Hosoi, Mari</creator><creator>Akai, Ryoko</creator><creator>Iwawaki, Takao</creator><creator>Ishikawa, Osamu</creator><creator>Motegi, Sei‐ichiro</creator><general>Wiley Subscription Services, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-2169-2427</orcidid><orcidid>https://orcid.org/0000-0002-7016-337X</orcidid><orcidid>https://orcid.org/0000-0001-8286-0669</orcidid></search><sort><creationdate>202107</creationdate><title>Inhibition of skin fibrosis in systemic sclerosis by botulinum toxin B via the suppression of oxidative stress</title><author>Baral, Hritu ; Sekiguchi, Akiko ; Uchiyama, Akihiko ; Nisaa Amalia, Syahla ; Yamazaki, Sahori ; Inoue, Yuta ; Yokoyama, Yoko ; Ogino, Sachiko ; Torii, Ryoko ; Hosoi, Mari ; Akai, Ryoko ; Iwawaki, Takao ; Ishikawa, Osamu ; Motegi, Sei‐ichiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4618-61b057bddd157095965ee290438ae57910ec35add3fa04933f144bba43b7d9dc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animal models</topic><topic>Apoptosis</topic><topic>Bioluminescence</topic><topic>Bleomycin</topic><topic>Botulinum toxin</topic><topic>Botulinum toxin type B</topic><topic>CYBB protein</topic><topic>fibroblast</topic><topic>Fibroblasts</topic><topic>Fibrosis</topic><topic>Inflammation</topic><topic>Injection</topic><topic>Injury prevention</topic><topic>Ischemia</topic><topic>mRNA</topic><topic>Oxidants</topic><topic>Oxidative stress</topic><topic>Reactive oxygen species</topic><topic>Reperfusion</topic><topic>Scars</topic><topic>Scleroderma</topic><topic>Skin diseases</topic><topic>skin fibrosis</topic><topic>Systemic sclerosis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Baral, Hritu</creatorcontrib><creatorcontrib>Sekiguchi, Akiko</creatorcontrib><creatorcontrib>Uchiyama, Akihiko</creatorcontrib><creatorcontrib>Nisaa Amalia, Syahla</creatorcontrib><creatorcontrib>Yamazaki, Sahori</creatorcontrib><creatorcontrib>Inoue, Yuta</creatorcontrib><creatorcontrib>Yokoyama, Yoko</creatorcontrib><creatorcontrib>Ogino, Sachiko</creatorcontrib><creatorcontrib>Torii, Ryoko</creatorcontrib><creatorcontrib>Hosoi, Mari</creatorcontrib><creatorcontrib>Akai, Ryoko</creatorcontrib><creatorcontrib>Iwawaki, Takao</creatorcontrib><creatorcontrib>Ishikawa, Osamu</creatorcontrib><creatorcontrib>Motegi, Sei‐ichiro</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of dermatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Baral, Hritu</au><au>Sekiguchi, Akiko</au><au>Uchiyama, Akihiko</au><au>Nisaa Amalia, Syahla</au><au>Yamazaki, Sahori</au><au>Inoue, Yuta</au><au>Yokoyama, Yoko</au><au>Ogino, Sachiko</au><au>Torii, Ryoko</au><au>Hosoi, Mari</au><au>Akai, Ryoko</au><au>Iwawaki, Takao</au><au>Ishikawa, Osamu</au><au>Motegi, Sei‐ichiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of skin fibrosis in systemic sclerosis by botulinum toxin B via the suppression of oxidative stress</atitle><jtitle>Journal of dermatology</jtitle><addtitle>J Dermatol</addtitle><date>2021-07</date><risdate>2021</risdate><volume>48</volume><issue>7</issue><spage>1052</spage><epage>1061</epage><pages>1052-1061</pages><issn>0385-2407</issn><eissn>1346-8138</eissn><abstract>Oxidative stress has been reported to play an important role in the pathogenesis of skin fibrosis in systemic sclerosis (SSc). We previously identified that botulinum toxin (BTX) injection suppresses pressure ulcer formation in a cutaneous ischemia–reperfusion injury mouse model by regulation of oxidative stress. However, the therapeutic possibility of BTX administration for preventing skin fibrosis in SSc is unclear. The objective of this study was to investigate the effect of BTX‐B on skin fibrosis in a murine model of SSc and determine the underlying mechanism. We found that BTX‐B injection significantly reduced dermal thickness and inflammatory cell infiltration in bleomycin‐induced skin fibrosis lesion in mice. We also identified that the oxidative stress signal detected through bioluminescence in OKD48 mice after bleomycin injection in the skin was significantly decreased by BTX‐B. Additionally, mRNA levels of oxidative stress associated factors (NOX2, HO‐1, Trx2) were significantly decreased by BTX‐B. Apoptotic cells in the lesional skin of bleomycin‐treated mice were significantly reduced by BTX‐B. Oxidant‐induced intracellular accumulation of reactive oxygen species in SSc fibroblasts was also inhibited by BTX‐B. In conclusion, BTX‐B might improve bleomycin‐induced skin fibrosis via the suppression of oxidative stress and inflammatory cells in the skin. BTX‐B injection may have a therapeutic effect on skin fibrosis in SSc.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>33840125</pmid><doi>10.1111/1346-8138.15888</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-2169-2427</orcidid><orcidid>https://orcid.org/0000-0002-7016-337X</orcidid><orcidid>https://orcid.org/0000-0001-8286-0669</orcidid></addata></record> |
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| source | Wiley Online Library Journals Frontfile Complete |
| subjects | Animal models Apoptosis Bioluminescence Bleomycin Botulinum toxin Botulinum toxin type B CYBB protein fibroblast Fibroblasts Fibrosis Inflammation Injection Injury prevention Ischemia mRNA Oxidants Oxidative stress Reactive oxygen species Reperfusion Scars Scleroderma Skin diseases skin fibrosis Systemic sclerosis |
| title | Inhibition of skin fibrosis in systemic sclerosis by botulinum toxin B via the suppression of oxidative stress |
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