Role of Kir4.1 Channels in Aminoglycoside-Induced Ototoxicity of Hair Cells
The Kir4.1 channel, an inwardly rectifying potassium ion (K+) channel, is located in the hair cells of the organ of Corti as well as the intermediate cells of the stria vascularis. The Kir4.1 channel has a crucial role in the generation of endolymphatic potential and maintenance of the resting membr...
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| creator | Choi, Jin Sil Ahn, Ye Ji Lee, SuHoon Park, Dong Jun Park, JeongEun Ha, Sun Mok Seo, Young Joon |
| description | The Kir4.1 channel, an inwardly rectifying potassium ion (K+) channel, is located in the hair cells of the organ of Corti as well as the intermediate cells of the stria vascularis. The Kir4.1 channel has a crucial role in the generation of endolymphatic potential and maintenance of the resting membrane potential. However, the role and functions of the Kir4.1 channel in the progenitor remain undescribed. To observe the role of Kir4.1 in the progenitor treated with the one-shot ototoxic drugs (kanamycin and furosemide), we set the proper condition in culturing Immortomouse-derived HEI-OC1 cells to express the potassium-related channels well. And also, that was reproduced in mice experiments to show the important role of Kir4.1 in the survival of hair cells after treating the ototoxicity drugs. In our results, when kanamycin and furosemide drugs were cotreated with HEI-OC1 cells, the Kir4.1 channel did not change, but the expression levels of the NKCC1 cotransporter and KCNQ4 channel are decreased. This shows that inward and outward channels were blocked by the two drugs (kanamycin and furosemide). However, noteworthy here is that the expression level of Kir4.1 channel increased when kanamycin was treated alone. This shows that Kir4.1, an inwardly rectifying potassium channel, acts as an outward channel in place of the corresponding channel when the KCNQ4 channel, an outward channel, is blocked. These results suggest that the Kir4.1 channel has a role in maintaining K+ homeostasis in supporting cells, with K+ concentration compensator when the NKCC1 cotransporter and Kv7.4 (KCNQ4) channels are deficient. |
| doi_str_mv | 10.1155/2023/4191999 |
| format | Article |
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The Kir4.1 channel has a crucial role in the generation of endolymphatic potential and maintenance of the resting membrane potential. However, the role and functions of the Kir4.1 channel in the progenitor remain undescribed. To observe the role of Kir4.1 in the progenitor treated with the one-shot ototoxic drugs (kanamycin and furosemide), we set the proper condition in culturing Immortomouse-derived HEI-OC1 cells to express the potassium-related channels well. And also, that was reproduced in mice experiments to show the important role of Kir4.1 in the survival of hair cells after treating the ototoxicity drugs. In our results, when kanamycin and furosemide drugs were cotreated with HEI-OC1 cells, the Kir4.1 channel did not change, but the expression levels of the NKCC1 cotransporter and KCNQ4 channel are decreased. This shows that inward and outward channels were blocked by the two drugs (kanamycin and furosemide). However, noteworthy here is that the expression level of Kir4.1 channel increased when kanamycin was treated alone. This shows that Kir4.1, an inwardly rectifying potassium channel, acts as an outward channel in place of the corresponding channel when the KCNQ4 channel, an outward channel, is blocked. These results suggest that the Kir4.1 channel has a role in maintaining K+ homeostasis in supporting cells, with K+ concentration compensator when the NKCC1 cotransporter and Kv7.4 (KCNQ4) channels are deficient.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2023/4191999</identifier><identifier>PMID: 38143588</identifier><language>eng</language><publisher>United States: Hindawi</publisher><subject>Aminoglycosides ; Aminoglycosides - toxicity ; Animals ; Anti-Bacterial Agents ; Antibiotics ; Ataxia ; Cell death ; Channels ; Chloride transport ; Compensators ; Drugs ; Furosemide ; Furosemide - pharmacology ; Hair ; Hair - metabolism ; Hair cells ; Hearing loss ; Hearing protection ; Homeostasis ; Kanamycin ; KCNQ4 protein ; Membrane potential ; Mice ; Mutation ; Organ of Corti ; Ototoxicity ; Potassium ; Potassium - metabolism ; Potassium channels (inwardly-rectifying) ; Potassium channels (voltage-gated) ; Potassium Channels, Inwardly Rectifying - metabolism ; Solute Carrier Family 12, Member 2 ; Stria vascularis ; Toxicity</subject><ispartof>BioMed research international, 2023, Vol.2023 (1), p.4191999-4191999</ispartof><rights>Copyright © 2023 Jin Sil Choi et al.</rights><rights>Copyright © 2023 Jin Sil Choi et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2023 Jin Sil Choi et al. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c449t-47ed05a2e7159660eaf43cc68fcf095e416d8c52a0fb98b7e65e73ec1b5774a23</citedby><cites>FETCH-LOGICAL-c449t-47ed05a2e7159660eaf43cc68fcf095e416d8c52a0fb98b7e65e73ec1b5774a23</cites><orcidid>0000-0002-2839-4676</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10748730/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10748730/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4010,27900,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38143588$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Siddiqui, Arif Jamal</contributor><contributor>Arif Jamal Siddiqui</contributor><creatorcontrib>Choi, Jin Sil</creatorcontrib><creatorcontrib>Ahn, Ye Ji</creatorcontrib><creatorcontrib>Lee, SuHoon</creatorcontrib><creatorcontrib>Park, Dong Jun</creatorcontrib><creatorcontrib>Park, JeongEun</creatorcontrib><creatorcontrib>Ha, Sun Mok</creatorcontrib><creatorcontrib>Seo, Young Joon</creatorcontrib><title>Role of Kir4.1 Channels in Aminoglycoside-Induced Ototoxicity of Hair Cells</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>The Kir4.1 channel, an inwardly rectifying potassium ion (K+) channel, is located in the hair cells of the organ of Corti as well as the intermediate cells of the stria vascularis. The Kir4.1 channel has a crucial role in the generation of endolymphatic potential and maintenance of the resting membrane potential. However, the role and functions of the Kir4.1 channel in the progenitor remain undescribed. To observe the role of Kir4.1 in the progenitor treated with the one-shot ototoxic drugs (kanamycin and furosemide), we set the proper condition in culturing Immortomouse-derived HEI-OC1 cells to express the potassium-related channels well. And also, that was reproduced in mice experiments to show the important role of Kir4.1 in the survival of hair cells after treating the ototoxicity drugs. In our results, when kanamycin and furosemide drugs were cotreated with HEI-OC1 cells, the Kir4.1 channel did not change, but the expression levels of the NKCC1 cotransporter and KCNQ4 channel are decreased. This shows that inward and outward channels were blocked by the two drugs (kanamycin and furosemide). However, noteworthy here is that the expression level of Kir4.1 channel increased when kanamycin was treated alone. This shows that Kir4.1, an inwardly rectifying potassium channel, acts as an outward channel in place of the corresponding channel when the KCNQ4 channel, an outward channel, is blocked. These results suggest that the Kir4.1 channel has a role in maintaining K+ homeostasis in supporting cells, with K+ concentration compensator when the NKCC1 cotransporter and Kv7.4 (KCNQ4) channels are deficient.</description><subject>Aminoglycosides</subject><subject>Aminoglycosides - toxicity</subject><subject>Animals</subject><subject>Anti-Bacterial Agents</subject><subject>Antibiotics</subject><subject>Ataxia</subject><subject>Cell death</subject><subject>Channels</subject><subject>Chloride transport</subject><subject>Compensators</subject><subject>Drugs</subject><subject>Furosemide</subject><subject>Furosemide - pharmacology</subject><subject>Hair</subject><subject>Hair - metabolism</subject><subject>Hair cells</subject><subject>Hearing loss</subject><subject>Hearing protection</subject><subject>Homeostasis</subject><subject>Kanamycin</subject><subject>KCNQ4 protein</subject><subject>Membrane potential</subject><subject>Mice</subject><subject>Mutation</subject><subject>Organ of Corti</subject><subject>Ototoxicity</subject><subject>Potassium</subject><subject>Potassium - metabolism</subject><subject>Potassium channels (inwardly-rectifying)</subject><subject>Potassium channels (voltage-gated)</subject><subject>Potassium Channels, Inwardly Rectifying - metabolism</subject><subject>Solute Carrier Family 12, Member 2</subject><subject>Stria vascularis</subject><subject>Toxicity</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kc1LAzEQxYMoKtqbZ1nwIuhqskk2yUmk-FEUBNFzSLOzNrJNNNlV-9-7tbWoB-cyA_ObxzweQnsEnxDC-WmBC3rKiCJKqTW0XVDC8pIwsr6aKd1Cg5SecV-SlFiVm2iLSsIol3Ib3dyHBrJQZzcushOSDSfGe2hS5nx2PnU-PDUzG5KrIB_5qrNQZXdtaMOHs66dzQ-vjYvZEJom7aKN2jQJBsu-gx4vLx6G1_nt3dVoeH6bW8ZUmzMBFeamAEG4KksMpmbU2lLWtsaKAyNlJS0vDK7HSo4FlBwEBUvGXAhmCrqDzha6L914CpUF30bT6JfopibOdDBO_954N9FP4U0TLJgUFPcKh0uFGF47SK2eumR7D8ZD6JIuFOZCFpyLHj34gz6HLvre3xdFFeOc99TxgrIxpBShXn1DsJ4npedJ6WVSPb7_08EK_s6lB44WwMT5yry7_-U-AQR7mag</recordid><startdate>2023</startdate><enddate>2023</enddate><creator>Choi, Jin Sil</creator><creator>Ahn, Ye Ji</creator><creator>Lee, SuHoon</creator><creator>Park, Dong Jun</creator><creator>Park, JeongEun</creator><creator>Ha, Sun Mok</creator><creator>Seo, Young Joon</creator><general>Hindawi</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</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>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-2839-4676</orcidid></search><sort><creationdate>2023</creationdate><title>Role of Kir4.1 Channels in Aminoglycoside-Induced Ototoxicity of Hair Cells</title><author>Choi, Jin Sil ; Ahn, Ye Ji ; Lee, SuHoon ; Park, Dong Jun ; Park, JeongEun ; Ha, Sun Mok ; Seo, Young Joon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c449t-47ed05a2e7159660eaf43cc68fcf095e416d8c52a0fb98b7e65e73ec1b5774a23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Aminoglycosides</topic><topic>Aminoglycosides - toxicity</topic><topic>Animals</topic><topic>Anti-Bacterial Agents</topic><topic>Antibiotics</topic><topic>Ataxia</topic><topic>Cell death</topic><topic>Channels</topic><topic>Chloride transport</topic><topic>Compensators</topic><topic>Drugs</topic><topic>Furosemide</topic><topic>Furosemide - pharmacology</topic><topic>Hair</topic><topic>Hair - metabolism</topic><topic>Hair cells</topic><topic>Hearing loss</topic><topic>Hearing protection</topic><topic>Homeostasis</topic><topic>Kanamycin</topic><topic>KCNQ4 protein</topic><topic>Membrane potential</topic><topic>Mice</topic><topic>Mutation</topic><topic>Organ of Corti</topic><topic>Ototoxicity</topic><topic>Potassium</topic><topic>Potassium - metabolism</topic><topic>Potassium channels (inwardly-rectifying)</topic><topic>Potassium channels (voltage-gated)</topic><topic>Potassium Channels, Inwardly Rectifying - metabolism</topic><topic>Solute Carrier Family 12, Member 2</topic><topic>Stria vascularis</topic><topic>Toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Choi, Jin Sil</creatorcontrib><creatorcontrib>Ahn, Ye Ji</creatorcontrib><creatorcontrib>Lee, SuHoon</creatorcontrib><creatorcontrib>Park, Dong Jun</creatorcontrib><creatorcontrib>Park, JeongEun</creatorcontrib><creatorcontrib>Ha, Sun Mok</creatorcontrib><creatorcontrib>Seo, Young Joon</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Advanced Technologies & Aerospace Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Middle East & Africa Database</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Choi, Jin Sil</au><au>Ahn, Ye Ji</au><au>Lee, SuHoon</au><au>Park, Dong Jun</au><au>Park, JeongEun</au><au>Ha, Sun Mok</au><au>Seo, Young Joon</au><au>Siddiqui, Arif Jamal</au><au>Arif Jamal Siddiqui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of Kir4.1 Channels in Aminoglycoside-Induced Ototoxicity of Hair Cells</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2023</date><risdate>2023</risdate><volume>2023</volume><issue>1</issue><spage>4191999</spage><epage>4191999</epage><pages>4191999-4191999</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>The Kir4.1 channel, an inwardly rectifying potassium ion (K+) channel, is located in the hair cells of the organ of Corti as well as the intermediate cells of the stria vascularis. The Kir4.1 channel has a crucial role in the generation of endolymphatic potential and maintenance of the resting membrane potential. However, the role and functions of the Kir4.1 channel in the progenitor remain undescribed. To observe the role of Kir4.1 in the progenitor treated with the one-shot ototoxic drugs (kanamycin and furosemide), we set the proper condition in culturing Immortomouse-derived HEI-OC1 cells to express the potassium-related channels well. And also, that was reproduced in mice experiments to show the important role of Kir4.1 in the survival of hair cells after treating the ototoxicity drugs. In our results, when kanamycin and furosemide drugs were cotreated with HEI-OC1 cells, the Kir4.1 channel did not change, but the expression levels of the NKCC1 cotransporter and KCNQ4 channel are decreased. This shows that inward and outward channels were blocked by the two drugs (kanamycin and furosemide). However, noteworthy here is that the expression level of Kir4.1 channel increased when kanamycin was treated alone. This shows that Kir4.1, an inwardly rectifying potassium channel, acts as an outward channel in place of the corresponding channel when the KCNQ4 channel, an outward channel, is blocked. These results suggest that the Kir4.1 channel has a role in maintaining K+ homeostasis in supporting cells, with K+ concentration compensator when the NKCC1 cotransporter and Kv7.4 (KCNQ4) channels are deficient.</abstract><cop>United States</cop><pub>Hindawi</pub><pmid>38143588</pmid><doi>10.1155/2023/4191999</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-2839-4676</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Aminoglycosides Aminoglycosides - toxicity Animals Anti-Bacterial Agents Antibiotics Ataxia Cell death Channels Chloride transport Compensators Drugs Furosemide Furosemide - pharmacology Hair Hair - metabolism Hair cells Hearing loss Hearing protection Homeostasis Kanamycin KCNQ4 protein Membrane potential Mice Mutation Organ of Corti Ototoxicity Potassium Potassium - metabolism Potassium channels (inwardly-rectifying) Potassium channels (voltage-gated) Potassium Channels, Inwardly Rectifying - metabolism Solute Carrier Family 12, Member 2 Stria vascularis Toxicity |
| title | Role of Kir4.1 Channels in Aminoglycoside-Induced Ototoxicity of Hair Cells |
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