d-Galactose-induced oxidative stress and mitochondrial dysfunction in the cochlear basilar membrane: an in vitro aging model
The cochlear basilar membrane (CBM) contains inner hair cells and outer hair cells that convert sound waves into electrical signals and transmit them to the central auditory system. Cochlear aging, the primary reason of age-related hearing loss, can reduce the signal transmission capacity. There is...
Gespeichert in:
| Veröffentlicht in: | Biogerontology (Dordrecht) 2020-06, Vol.21 (3), p.311-323 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 323 |
|---|---|
| container_issue | 3 |
| container_start_page | 311 |
| container_title | Biogerontology (Dordrecht) |
| container_volume | 21 |
| creator | Guo, Bin Guo, Qing Wang, Zhan Shao, Jian-Bo Liu, Ke Du, Zheng-De Gong, Shu-Sheng |
| description | The cochlear basilar membrane (CBM) contains inner hair cells and outer hair cells that convert sound waves into electrical signals and transmit them to the central auditory system. Cochlear aging, the primary reason of age-related hearing loss, can reduce the signal transmission capacity. There is no ideal in vitro aging model of the CBM. In this study, we cultured the CBM, which was dissected from the cochlea of the C57BL/6 mice 5 days after birth, in a medium containing 20 mg/mL, 40 mg/mL, or 60 mg/mL
d
-galactose (
d
-gal). Compared with the control group, the levels of senescence-associated β-galactosidase were increased in a concentration-dependent manner in the CBM of the
d
-gal groups. In addition, levels of the mitochondrial superoxide and patterns of an age-related mitochondrial DNA3860-bp deletion were significantly increased. The ATP levels and the membrane potential of the mitochondrial were significantly decreased in the CBM of the D-gal groups compared with the control group. Furthermore, in comparison with the control group, damaged hair cell stereocilia and a loss of inner hair cell ribbon synapses were observed in the CBM of the
d
-gal groups. A loss of hair cells and activation of caspase-3-mediated outer hair cell apoptosis were also observed in the CBM of the high-dose
d
-gal group. These insults induced by D-gal in the CBM in vitro were similar to the ones that occur in cochlear natural aging in vivo. Thus, we believe that this is a successful in vitro aging model using cultured CBM. These results demonstrate the effects of mitochondrial oxidative damage on presbycusis and provide a reliable aging model to study the mechanisms of presbycusis in vitro. |
| doi_str_mv | 10.1007/s10522-020-09859-x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7196095</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2397280669</sourcerecordid><originalsourceid>FETCH-LOGICAL-c540t-a6191a2e6abffc365612ea454527766d0a846cc640baf848a76b091d2974f64d3</originalsourceid><addsrcrecordid>eNp9kc1rFTEUxQdRbK3-Ay4k4MZNNMnkY-JCKMVWoeBG1-FOknkvZSapSebxCv7xpn21fixc3cD9nZN7OF33kpK3lBD1rlAiGMOEEUz0IDTeP-qOqVA9lkoOj9u7HzQWiumj7lkpV4RQyaR42h31jDDJiD7ufjh8ATPYmorHIbrVeofSPjioYedRqdmXgiA6tISa7DZFlwPMyN2UaY22hhRRiKhuPbJtPXvIaIQS5jYXv4wZon_f9LfQLtScEGxC3KAlOT8_755MMBf_4n6edN_OP349-4Qvv1x8Pju9xFZwUjFIqikwL2GcJttLISnzwAUXTCkpHYGBS2slJyNMAx9AyZFo6phWfJLc9Sfdh4Pv9Tou3lkfa4bZXOewQL4xCYL5exPD1mzSziiqJdGiGby5N8jp--pLNUso1s9zS5fWYlgvGBE9H3hDX_-DXqU1xxavUVqxgUipG8UOlM2plOynh2MoMbflmkO5ppVr7so1-yZ69WeMB8mvNhvQH4DSVnHj8--__2P7E08psqo</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2397280669</pqid></control><display><type>article</type><title>d-Galactose-induced oxidative stress and mitochondrial dysfunction in the cochlear basilar membrane: an in vitro aging model</title><source>SpringerNature Journals</source><creator>Guo, Bin ; Guo, Qing ; Wang, Zhan ; Shao, Jian-Bo ; Liu, Ke ; Du, Zheng-De ; Gong, Shu-Sheng</creator><creatorcontrib>Guo, Bin ; Guo, Qing ; Wang, Zhan ; Shao, Jian-Bo ; Liu, Ke ; Du, Zheng-De ; Gong, Shu-Sheng</creatorcontrib><description>The cochlear basilar membrane (CBM) contains inner hair cells and outer hair cells that convert sound waves into electrical signals and transmit them to the central auditory system. Cochlear aging, the primary reason of age-related hearing loss, can reduce the signal transmission capacity. There is no ideal in vitro aging model of the CBM. In this study, we cultured the CBM, which was dissected from the cochlea of the C57BL/6 mice 5 days after birth, in a medium containing 20 mg/mL, 40 mg/mL, or 60 mg/mL
d
-galactose (
d
-gal). Compared with the control group, the levels of senescence-associated β-galactosidase were increased in a concentration-dependent manner in the CBM of the
d
-gal groups. In addition, levels of the mitochondrial superoxide and patterns of an age-related mitochondrial DNA3860-bp deletion were significantly increased. The ATP levels and the membrane potential of the mitochondrial were significantly decreased in the CBM of the D-gal groups compared with the control group. Furthermore, in comparison with the control group, damaged hair cell stereocilia and a loss of inner hair cell ribbon synapses were observed in the CBM of the
d
-gal groups. A loss of hair cells and activation of caspase-3-mediated outer hair cell apoptosis were also observed in the CBM of the high-dose
d
-gal group. These insults induced by D-gal in the CBM in vitro were similar to the ones that occur in cochlear natural aging in vivo. Thus, we believe that this is a successful in vitro aging model using cultured CBM. These results demonstrate the effects of mitochondrial oxidative damage on presbycusis and provide a reliable aging model to study the mechanisms of presbycusis in vitro.</description><identifier>ISSN: 1389-5729</identifier><identifier>EISSN: 1573-6768</identifier><identifier>DOI: 10.1007/s10522-020-09859-x</identifier><identifier>PMID: 32026209</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Aging ; Apoptosis ; Auditory system ; Biomedical and Life Sciences ; Caspase-3 ; Cell activation ; Cell Biology ; Cochlea ; D-Galactose ; Developmental Biology ; Galactose ; Gene deletion ; Geriatrics/Gerontology ; Hair cells ; Hearing loss ; Life Sciences ; Membrane potential ; Mitochondria ; Outer hair cells ; Oxidative stress ; Research Article ; Senescence ; Superoxide ; Synapses ; Synaptic ribbons ; β-Galactosidase</subject><ispartof>Biogerontology (Dordrecht), 2020-06, Vol.21 (3), p.311-323</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c540t-a6191a2e6abffc365612ea454527766d0a846cc640baf848a76b091d2974f64d3</citedby><cites>FETCH-LOGICAL-c540t-a6191a2e6abffc365612ea454527766d0a846cc640baf848a76b091d2974f64d3</cites><orcidid>0000-0001-7885-7731</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10522-020-09859-x$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10522-020-09859-x$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32026209$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guo, Bin</creatorcontrib><creatorcontrib>Guo, Qing</creatorcontrib><creatorcontrib>Wang, Zhan</creatorcontrib><creatorcontrib>Shao, Jian-Bo</creatorcontrib><creatorcontrib>Liu, Ke</creatorcontrib><creatorcontrib>Du, Zheng-De</creatorcontrib><creatorcontrib>Gong, Shu-Sheng</creatorcontrib><title>d-Galactose-induced oxidative stress and mitochondrial dysfunction in the cochlear basilar membrane: an in vitro aging model</title><title>Biogerontology (Dordrecht)</title><addtitle>Biogerontology</addtitle><addtitle>Biogerontology</addtitle><description>The cochlear basilar membrane (CBM) contains inner hair cells and outer hair cells that convert sound waves into electrical signals and transmit them to the central auditory system. Cochlear aging, the primary reason of age-related hearing loss, can reduce the signal transmission capacity. There is no ideal in vitro aging model of the CBM. In this study, we cultured the CBM, which was dissected from the cochlea of the C57BL/6 mice 5 days after birth, in a medium containing 20 mg/mL, 40 mg/mL, or 60 mg/mL
d
-galactose (
d
-gal). Compared with the control group, the levels of senescence-associated β-galactosidase were increased in a concentration-dependent manner in the CBM of the
d
-gal groups. In addition, levels of the mitochondrial superoxide and patterns of an age-related mitochondrial DNA3860-bp deletion were significantly increased. The ATP levels and the membrane potential of the mitochondrial were significantly decreased in the CBM of the D-gal groups compared with the control group. Furthermore, in comparison with the control group, damaged hair cell stereocilia and a loss of inner hair cell ribbon synapses were observed in the CBM of the
d
-gal groups. A loss of hair cells and activation of caspase-3-mediated outer hair cell apoptosis were also observed in the CBM of the high-dose
d
-gal group. These insults induced by D-gal in the CBM in vitro were similar to the ones that occur in cochlear natural aging in vivo. Thus, we believe that this is a successful in vitro aging model using cultured CBM. These results demonstrate the effects of mitochondrial oxidative damage on presbycusis and provide a reliable aging model to study the mechanisms of presbycusis in vitro.</description><subject>Aging</subject><subject>Apoptosis</subject><subject>Auditory system</subject><subject>Biomedical and Life Sciences</subject><subject>Caspase-3</subject><subject>Cell activation</subject><subject>Cell Biology</subject><subject>Cochlea</subject><subject>D-Galactose</subject><subject>Developmental Biology</subject><subject>Galactose</subject><subject>Gene deletion</subject><subject>Geriatrics/Gerontology</subject><subject>Hair cells</subject><subject>Hearing loss</subject><subject>Life Sciences</subject><subject>Membrane potential</subject><subject>Mitochondria</subject><subject>Outer hair cells</subject><subject>Oxidative stress</subject><subject>Research Article</subject><subject>Senescence</subject><subject>Superoxide</subject><subject>Synapses</subject><subject>Synaptic ribbons</subject><subject>β-Galactosidase</subject><issn>1389-5729</issn><issn>1573-6768</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc1rFTEUxQdRbK3-Ay4k4MZNNMnkY-JCKMVWoeBG1-FOknkvZSapSebxCv7xpn21fixc3cD9nZN7OF33kpK3lBD1rlAiGMOEEUz0IDTeP-qOqVA9lkoOj9u7HzQWiumj7lkpV4RQyaR42h31jDDJiD7ufjh8ATPYmorHIbrVeofSPjioYedRqdmXgiA6tISa7DZFlwPMyN2UaY22hhRRiKhuPbJtPXvIaIQS5jYXv4wZon_f9LfQLtScEGxC3KAlOT8_755MMBf_4n6edN_OP349-4Qvv1x8Pju9xFZwUjFIqikwL2GcJttLISnzwAUXTCkpHYGBS2slJyNMAx9AyZFo6phWfJLc9Sfdh4Pv9Tou3lkfa4bZXOewQL4xCYL5exPD1mzSziiqJdGiGby5N8jp--pLNUso1s9zS5fWYlgvGBE9H3hDX_-DXqU1xxavUVqxgUipG8UOlM2plOynh2MoMbflmkO5ppVr7so1-yZ69WeMB8mvNhvQH4DSVnHj8--__2P7E08psqo</recordid><startdate>20200601</startdate><enddate>20200601</enddate><creator>Guo, Bin</creator><creator>Guo, Qing</creator><creator>Wang, Zhan</creator><creator>Shao, Jian-Bo</creator><creator>Liu, Ke</creator><creator>Du, Zheng-De</creator><creator>Gong, Shu-Sheng</creator><general>Springer Netherlands</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>0-V</scope><scope>3V.</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88J</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ALSLI</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2R</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7885-7731</orcidid></search><sort><creationdate>20200601</creationdate><title>d-Galactose-induced oxidative stress and mitochondrial dysfunction in the cochlear basilar membrane: an in vitro aging model</title><author>Guo, Bin ; Guo, Qing ; Wang, Zhan ; Shao, Jian-Bo ; Liu, Ke ; Du, Zheng-De ; Gong, Shu-Sheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c540t-a6191a2e6abffc365612ea454527766d0a846cc640baf848a76b091d2974f64d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Aging</topic><topic>Apoptosis</topic><topic>Auditory system</topic><topic>Biomedical and Life Sciences</topic><topic>Caspase-3</topic><topic>Cell activation</topic><topic>Cell Biology</topic><topic>Cochlea</topic><topic>D-Galactose</topic><topic>Developmental Biology</topic><topic>Galactose</topic><topic>Gene deletion</topic><topic>Geriatrics/Gerontology</topic><topic>Hair cells</topic><topic>Hearing loss</topic><topic>Life Sciences</topic><topic>Membrane potential</topic><topic>Mitochondria</topic><topic>Outer hair cells</topic><topic>Oxidative stress</topic><topic>Research Article</topic><topic>Senescence</topic><topic>Superoxide</topic><topic>Synapses</topic><topic>Synaptic ribbons</topic><topic>β-Galactosidase</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guo, Bin</creatorcontrib><creatorcontrib>Guo, Qing</creatorcontrib><creatorcontrib>Wang, Zhan</creatorcontrib><creatorcontrib>Shao, Jian-Bo</creatorcontrib><creatorcontrib>Liu, Ke</creatorcontrib><creatorcontrib>Du, Zheng-De</creatorcontrib><creatorcontrib>Gong, Shu-Sheng</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Social Sciences Premium Collection</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Social Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Social Science Premium Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Social Science Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Biogerontology (Dordrecht)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guo, Bin</au><au>Guo, Qing</au><au>Wang, Zhan</au><au>Shao, Jian-Bo</au><au>Liu, Ke</au><au>Du, Zheng-De</au><au>Gong, Shu-Sheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>d-Galactose-induced oxidative stress and mitochondrial dysfunction in the cochlear basilar membrane: an in vitro aging model</atitle><jtitle>Biogerontology (Dordrecht)</jtitle><stitle>Biogerontology</stitle><addtitle>Biogerontology</addtitle><date>2020-06-01</date><risdate>2020</risdate><volume>21</volume><issue>3</issue><spage>311</spage><epage>323</epage><pages>311-323</pages><issn>1389-5729</issn><eissn>1573-6768</eissn><abstract>The cochlear basilar membrane (CBM) contains inner hair cells and outer hair cells that convert sound waves into electrical signals and transmit them to the central auditory system. Cochlear aging, the primary reason of age-related hearing loss, can reduce the signal transmission capacity. There is no ideal in vitro aging model of the CBM. In this study, we cultured the CBM, which was dissected from the cochlea of the C57BL/6 mice 5 days after birth, in a medium containing 20 mg/mL, 40 mg/mL, or 60 mg/mL
d
-galactose (
d
-gal). Compared with the control group, the levels of senescence-associated β-galactosidase were increased in a concentration-dependent manner in the CBM of the
d
-gal groups. In addition, levels of the mitochondrial superoxide and patterns of an age-related mitochondrial DNA3860-bp deletion were significantly increased. The ATP levels and the membrane potential of the mitochondrial were significantly decreased in the CBM of the D-gal groups compared with the control group. Furthermore, in comparison with the control group, damaged hair cell stereocilia and a loss of inner hair cell ribbon synapses were observed in the CBM of the
d
-gal groups. A loss of hair cells and activation of caspase-3-mediated outer hair cell apoptosis were also observed in the CBM of the high-dose
d
-gal group. These insults induced by D-gal in the CBM in vitro were similar to the ones that occur in cochlear natural aging in vivo. Thus, we believe that this is a successful in vitro aging model using cultured CBM. These results demonstrate the effects of mitochondrial oxidative damage on presbycusis and provide a reliable aging model to study the mechanisms of presbycusis in vitro.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>32026209</pmid><doi>10.1007/s10522-020-09859-x</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-7885-7731</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1389-5729 |
| ispartof | Biogerontology (Dordrecht), 2020-06, Vol.21 (3), p.311-323 |
| issn | 1389-5729 1573-6768 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7196095 |
| source | SpringerNature Journals |
| subjects | Aging Apoptosis Auditory system Biomedical and Life Sciences Caspase-3 Cell activation Cell Biology Cochlea D-Galactose Developmental Biology Galactose Gene deletion Geriatrics/Gerontology Hair cells Hearing loss Life Sciences Membrane potential Mitochondria Outer hair cells Oxidative stress Research Article Senescence Superoxide Synapses Synaptic ribbons β-Galactosidase |
| title | d-Galactose-induced oxidative stress and mitochondrial dysfunction in the cochlear basilar membrane: an in vitro aging model |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-26T02%3A41%3A14IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=d-Galactose-induced%20oxidative%20stress%20and%20mitochondrial%20dysfunction%20in%20the%20cochlear%20basilar%20membrane:%20an%20in%20vitro%20aging%20model&rft.jtitle=Biogerontology%20(Dordrecht)&rft.au=Guo,%20Bin&rft.date=2020-06-01&rft.volume=21&rft.issue=3&rft.spage=311&rft.epage=323&rft.pages=311-323&rft.issn=1389-5729&rft.eissn=1573-6768&rft_id=info:doi/10.1007/s10522-020-09859-x&rft_dat=%3Cproquest_pubme%3E2397280669%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2397280669&rft_id=info:pmid/32026209&rfr_iscdi=true |