Self-protection of type III fibrocytes against severe 3-nitropropionic-acid-induced cochlear damage in mice
After intense sound exposure, the lack of obvious degeneration in type III fibrocytes suggests that they might protect themselves against acoustic trauma. However, it is unknown whether and how type III fibrocytes play this role in other cochlear damage models. In this study, we investigated the sel...
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| Veröffentlicht in: | Neuroreport 2018-03, Vol.29 (4), p.252-258 |
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| creator | Li, Yang Sheng, Ying Liang, Jian-Min Hu, Juan Ren, Xiao-Yong Cheng, Yan |
| description | After intense sound exposure, the lack of obvious degeneration in type III fibrocytes suggests that they might protect themselves against acoustic trauma. However, it is unknown whether and how type III fibrocytes play this role in other cochlear damage models. In this study, we investigated the self-protection of type III fibrocytes against severe cochlear energy failure induced by local administration of 3-nitropropionic acid to the inner ear. We detected that the type III fibrocytes did not degenerate significantly after 500 mM 3-nitropropionic acid application, and showed increased expression of proliferation marker Ki67. Moreover, low immunoreactivity for inducible nitric oxide synthase and cleaved caspase-3 was observed in type III fibrocytes 2 days after damage. These results indicate that after severe cochlear energy failure type III fibrocytes possess obvious proliferation activity, as well as strong antioxidant and antiapoptotic capacity, which can protect them from degeneration. |
| doi_str_mv | 10.1097/WNR.0000000000000927 |
| format | Article |
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However, it is unknown whether and how type III fibrocytes play this role in other cochlear damage models. In this study, we investigated the self-protection of type III fibrocytes against severe cochlear energy failure induced by local administration of 3-nitropropionic acid to the inner ear. We detected that the type III fibrocytes did not degenerate significantly after 500 mM 3-nitropropionic acid application, and showed increased expression of proliferation marker Ki67. Moreover, low immunoreactivity for inducible nitric oxide synthase and cleaved caspase-3 was observed in type III fibrocytes 2 days after damage. These results indicate that after severe cochlear energy failure type III fibrocytes possess obvious proliferation activity, as well as strong antioxidant and antiapoptotic capacity, which can protect them from degeneration.</description><identifier>ISSN: 0959-4965</identifier><identifier>EISSN: 1473-558X</identifier><identifier>DOI: 10.1097/WNR.0000000000000927</identifier><identifier>PMID: 29280748</identifier><language>eng</language><publisher>England: Wolters Kluwer Health | Lippincott Williams & Wilkins</publisher><subject>Animals ; Apoptosis - drug effects ; Apoptosis - physiology ; Aquaporin 1 - metabolism ; Caspase 3 - metabolism ; Cell Proliferation - drug effects ; Cell Proliferation - physiology ; Cochlea - drug effects ; Cochlea - metabolism ; Cochlea - pathology ; Cochlear Diseases - chemically induced ; Cochlear Diseases - metabolism ; Cochlear Diseases - pathology ; Evoked Potentials, Auditory, Brain Stem - drug effects ; Gene Expression - drug effects ; Ki-67 Antigen - metabolism ; Male ; Mice, Inbred C57BL ; Nerve Degeneration - chemically induced ; Nerve Degeneration - metabolism ; Nerve Degeneration - pathology ; Nitric Oxide Synthase Type II - metabolism ; Nitro Compounds - adverse effects ; Oxidative Stress - drug effects ; Oxidative Stress - physiology ; Propionates - adverse effects</subject><ispartof>Neuroreport, 2018-03, Vol.29 (4), p.252-258</ispartof><rights>2017 Wolters Kluwer Health | Lippincott Williams & Wilkins</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3567-937a92f7d45ef4f17389c09379f4040dde8418134e1c569446c7198aa455907d3</citedby><cites>FETCH-LOGICAL-c3567-937a92f7d45ef4f17389c09379f4040dde8418134e1c569446c7198aa455907d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29280748$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Yang</creatorcontrib><creatorcontrib>Sheng, Ying</creatorcontrib><creatorcontrib>Liang, Jian-Min</creatorcontrib><creatorcontrib>Hu, Juan</creatorcontrib><creatorcontrib>Ren, Xiao-Yong</creatorcontrib><creatorcontrib>Cheng, Yan</creatorcontrib><title>Self-protection of type III fibrocytes against severe 3-nitropropionic-acid-induced cochlear damage in mice</title><title>Neuroreport</title><addtitle>Neuroreport</addtitle><description>After intense sound exposure, the lack of obvious degeneration in type III fibrocytes suggests that they might protect themselves against acoustic trauma. However, it is unknown whether and how type III fibrocytes play this role in other cochlear damage models. In this study, we investigated the self-protection of type III fibrocytes against severe cochlear energy failure induced by local administration of 3-nitropropionic acid to the inner ear. We detected that the type III fibrocytes did not degenerate significantly after 500 mM 3-nitropropionic acid application, and showed increased expression of proliferation marker Ki67. Moreover, low immunoreactivity for inducible nitric oxide synthase and cleaved caspase-3 was observed in type III fibrocytes 2 days after damage. These results indicate that after severe cochlear energy failure type III fibrocytes possess obvious proliferation activity, as well as strong antioxidant and antiapoptotic capacity, which can protect them from degeneration.</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Aquaporin 1 - metabolism</subject><subject>Caspase 3 - metabolism</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Proliferation - physiology</subject><subject>Cochlea - drug effects</subject><subject>Cochlea - metabolism</subject><subject>Cochlea - pathology</subject><subject>Cochlear Diseases - chemically induced</subject><subject>Cochlear Diseases - metabolism</subject><subject>Cochlear Diseases - pathology</subject><subject>Evoked Potentials, Auditory, Brain Stem - drug effects</subject><subject>Gene Expression - drug effects</subject><subject>Ki-67 Antigen - metabolism</subject><subject>Male</subject><subject>Mice, Inbred C57BL</subject><subject>Nerve Degeneration - chemically induced</subject><subject>Nerve Degeneration - metabolism</subject><subject>Nerve Degeneration - pathology</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Nitro Compounds - adverse effects</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidative Stress - physiology</subject><subject>Propionates - adverse effects</subject><issn>0959-4965</issn><issn>1473-558X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kFFLHDEQx0NR6mn7DYrk0Zdocptsksci2h6IglratyUmEy-6uzmTbI_79s1xKqUPnZeB4fefGX4IfWH0lFEtz35e357Sv0vP5Qc0Y1w2RAj1aw_NqBaacN2KA3SY89OWoUx9RAdzPVdUcjVDz3fQe7JKsYAtIY44elw2K8CLxQL78JCi3RTI2DyaMOaCM_yGBLghYygp1tyqhoIlxgZHwugmCw7baJc9mISdGcwj4DDiIVj4hPa96TN8fu1H6Mflxf35d3J1821x_vWK2Ea0kuhGGj330nEBnnsmG6UtrVPtOeXUOVCcKdZwYFa0mvPWSqaVMVwITaVrjtDJbm9972WCXLohZAt9b0aIU-4qzKjgrWAV5TvUpphzAt-tUhhM2nSMdlvNXdXc_au5xo5fL0wPA7j30JvXCqgdsI59gZSf-2kNqVuC6cvy_7v_AP29iR8</recordid><startdate>20180307</startdate><enddate>20180307</enddate><creator>Li, Yang</creator><creator>Sheng, Ying</creator><creator>Liang, Jian-Min</creator><creator>Hu, Juan</creator><creator>Ren, Xiao-Yong</creator><creator>Cheng, Yan</creator><general>Wolters Kluwer Health | Lippincott Williams & Wilkins</general><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>7X8</scope></search><sort><creationdate>20180307</creationdate><title>Self-protection of type III fibrocytes against severe 3-nitropropionic-acid-induced cochlear damage in mice</title><author>Li, Yang ; Sheng, Ying ; Liang, Jian-Min ; Hu, Juan ; Ren, Xiao-Yong ; Cheng, Yan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3567-937a92f7d45ef4f17389c09379f4040dde8418134e1c569446c7198aa455907d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Aquaporin 1 - metabolism</topic><topic>Caspase 3 - metabolism</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Proliferation - physiology</topic><topic>Cochlea - drug effects</topic><topic>Cochlea - metabolism</topic><topic>Cochlea - pathology</topic><topic>Cochlear Diseases - chemically induced</topic><topic>Cochlear Diseases - metabolism</topic><topic>Cochlear Diseases - pathology</topic><topic>Evoked Potentials, Auditory, Brain Stem - drug effects</topic><topic>Gene Expression - drug effects</topic><topic>Ki-67 Antigen - metabolism</topic><topic>Male</topic><topic>Mice, Inbred C57BL</topic><topic>Nerve Degeneration - chemically induced</topic><topic>Nerve Degeneration - metabolism</topic><topic>Nerve Degeneration - pathology</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Nitro Compounds - adverse effects</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidative Stress - physiology</topic><topic>Propionates - adverse effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Yang</creatorcontrib><creatorcontrib>Sheng, Ying</creatorcontrib><creatorcontrib>Liang, Jian-Min</creatorcontrib><creatorcontrib>Hu, Juan</creatorcontrib><creatorcontrib>Ren, Xiao-Yong</creatorcontrib><creatorcontrib>Cheng, Yan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroreport</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Yang</au><au>Sheng, Ying</au><au>Liang, Jian-Min</au><au>Hu, Juan</au><au>Ren, Xiao-Yong</au><au>Cheng, Yan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Self-protection of type III fibrocytes against severe 3-nitropropionic-acid-induced cochlear damage in mice</atitle><jtitle>Neuroreport</jtitle><addtitle>Neuroreport</addtitle><date>2018-03-07</date><risdate>2018</risdate><volume>29</volume><issue>4</issue><spage>252</spage><epage>258</epage><pages>252-258</pages><issn>0959-4965</issn><eissn>1473-558X</eissn><abstract>After intense sound exposure, the lack of obvious degeneration in type III fibrocytes suggests that they might protect themselves against acoustic trauma. However, it is unknown whether and how type III fibrocytes play this role in other cochlear damage models. In this study, we investigated the self-protection of type III fibrocytes against severe cochlear energy failure induced by local administration of 3-nitropropionic acid to the inner ear. We detected that the type III fibrocytes did not degenerate significantly after 500 mM 3-nitropropionic acid application, and showed increased expression of proliferation marker Ki67. Moreover, low immunoreactivity for inducible nitric oxide synthase and cleaved caspase-3 was observed in type III fibrocytes 2 days after damage. These results indicate that after severe cochlear energy failure type III fibrocytes possess obvious proliferation activity, as well as strong antioxidant and antiapoptotic capacity, which can protect them from degeneration.</abstract><cop>England</cop><pub>Wolters Kluwer Health | Lippincott Williams & Wilkins</pub><pmid>29280748</pmid><doi>10.1097/WNR.0000000000000927</doi><tpages>7</tpages></addata></record> |
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| subjects | Animals Apoptosis - drug effects Apoptosis - physiology Aquaporin 1 - metabolism Caspase 3 - metabolism Cell Proliferation - drug effects Cell Proliferation - physiology Cochlea - drug effects Cochlea - metabolism Cochlea - pathology Cochlear Diseases - chemically induced Cochlear Diseases - metabolism Cochlear Diseases - pathology Evoked Potentials, Auditory, Brain Stem - drug effects Gene Expression - drug effects Ki-67 Antigen - metabolism Male Mice, Inbred C57BL Nerve Degeneration - chemically induced Nerve Degeneration - metabolism Nerve Degeneration - pathology Nitric Oxide Synthase Type II - metabolism Nitro Compounds - adverse effects Oxidative Stress - drug effects Oxidative Stress - physiology Propionates - adverse effects |
| title | Self-protection of type III fibrocytes against severe 3-nitropropionic-acid-induced cochlear damage in mice |
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