Chemerin/CMKLR1 pathway exacerbates cisplatin-induced spiral ganglion neuron injury
Abstract This study investigated whether chemerin/chemokine-like receptor 1 (CMKLR1) pathway participate in cisplatin‐induced spiral ganglion neuron (SGN) damage. Middle cochlear turn was collected from C57BL/6 mice and the SGNs were cultured. Cisplatin, 2-(anaphthoyl) ethyltrimethylammonium iodide...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Tian, Jie [verfasserIn] |
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E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2023 |
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| Anmerkung: |
© The Author(s) under exclusive licence to Korean Society of Toxicology 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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| Übergeordnetes Werk: |
Enthalten in: Toxicological research - Seoul : Soc., 2008, 40(2023), 1 vom: 24. Aug., Seite 73-81 |
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| Übergeordnetes Werk: |
volume:40 ; year:2023 ; number:1 ; day:24 ; month:08 ; pages:73-81 |
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| DOI / URN: |
10.1007/s43188-023-00205-0 |
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SPR054377919 |
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| 520 | |a Abstract This study investigated whether chemerin/chemokine-like receptor 1 (CMKLR1) pathway participate in cisplatin‐induced spiral ganglion neuron (SGN) damage. Middle cochlear turn was collected from C57BL/6 mice and the SGNs were cultured. Cisplatin, 2-(anaphthoyl) ethyltrimethylammonium iodide (α-NETA), or recombinant mouse chemerin was added into the medium for the treatment. Relative mRNA and protein expression was determined by RT-PCR, ELISA and Western blot, respectively. In cultured mouse cochlear SGNs, the treatment of cisplatin enhanced the secretion of chemerin and CMKLR1. Recombinant chemerin promoted but α-NETA inhibited chemerin/CMKLR1 pathway in cisplatin stimulated SGNs. Cisplatin-induced apoptosis and inflammation response in SGNs were enhanced by recombinant chemerin while inhibited by α-NETA. Recombinant chemerin promoted but α-NETA inhibited NF-κB signal in cisplatin stimulated SGNs. In conclusion, chemerin/CMKLR1 pathway regulated apoptosis and inflammation response in cisplatin-induced SGN injury through NF-κB signaling pathway. | ||
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10.1007/s43188-023-00205-0 doi (DE-627)SPR054377919 (SPR)s43188-023-00205-0-e DE-627 ger DE-627 rakwb eng Tian, Jie verfasserin aut Chemerin/CMKLR1 pathway exacerbates cisplatin-induced spiral ganglion neuron injury 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) under exclusive licence to Korean Society of Toxicology 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract This study investigated whether chemerin/chemokine-like receptor 1 (CMKLR1) pathway participate in cisplatin‐induced spiral ganglion neuron (SGN) damage. Middle cochlear turn was collected from C57BL/6 mice and the SGNs were cultured. Cisplatin, 2-(anaphthoyl) ethyltrimethylammonium iodide (α-NETA), or recombinant mouse chemerin was added into the medium for the treatment. Relative mRNA and protein expression was determined by RT-PCR, ELISA and Western blot, respectively. In cultured mouse cochlear SGNs, the treatment of cisplatin enhanced the secretion of chemerin and CMKLR1. Recombinant chemerin promoted but α-NETA inhibited chemerin/CMKLR1 pathway in cisplatin stimulated SGNs. Cisplatin-induced apoptosis and inflammation response in SGNs were enhanced by recombinant chemerin while inhibited by α-NETA. Recombinant chemerin promoted but α-NETA inhibited NF-κB signal in cisplatin stimulated SGNs. In conclusion, chemerin/CMKLR1 pathway regulated apoptosis and inflammation response in cisplatin-induced SGN injury through NF-κB signaling pathway. Chemerin (dpeaa)DE-He213 CMKLR1 (dpeaa)DE-He213 Cisplatin (dpeaa)DE-He213 Spiral ganglion neuron (dpeaa)DE-He213 Injury (dpeaa)DE-He213 Mu, Ying aut Ma, Lili (orcid)0000-0002-2679-9397 aut Enthalten in Toxicological research Seoul : Soc., 2008 40(2023), 1 vom: 24. Aug., Seite 73-81 (DE-627)757130194 (DE-600)2727978-9 2234-2753 nnns volume:40 year:2023 number:1 day:24 month:08 pages:73-81 https://dx.doi.org/10.1007/s43188-023-00205-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 40 2023 1 24 08 73-81 |
| spelling |
10.1007/s43188-023-00205-0 doi (DE-627)SPR054377919 (SPR)s43188-023-00205-0-e DE-627 ger DE-627 rakwb eng Tian, Jie verfasserin aut Chemerin/CMKLR1 pathway exacerbates cisplatin-induced spiral ganglion neuron injury 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) under exclusive licence to Korean Society of Toxicology 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract This study investigated whether chemerin/chemokine-like receptor 1 (CMKLR1) pathway participate in cisplatin‐induced spiral ganglion neuron (SGN) damage. Middle cochlear turn was collected from C57BL/6 mice and the SGNs were cultured. Cisplatin, 2-(anaphthoyl) ethyltrimethylammonium iodide (α-NETA), or recombinant mouse chemerin was added into the medium for the treatment. Relative mRNA and protein expression was determined by RT-PCR, ELISA and Western blot, respectively. In cultured mouse cochlear SGNs, the treatment of cisplatin enhanced the secretion of chemerin and CMKLR1. Recombinant chemerin promoted but α-NETA inhibited chemerin/CMKLR1 pathway in cisplatin stimulated SGNs. Cisplatin-induced apoptosis and inflammation response in SGNs were enhanced by recombinant chemerin while inhibited by α-NETA. Recombinant chemerin promoted but α-NETA inhibited NF-κB signal in cisplatin stimulated SGNs. In conclusion, chemerin/CMKLR1 pathway regulated apoptosis and inflammation response in cisplatin-induced SGN injury through NF-κB signaling pathway. Chemerin (dpeaa)DE-He213 CMKLR1 (dpeaa)DE-He213 Cisplatin (dpeaa)DE-He213 Spiral ganglion neuron (dpeaa)DE-He213 Injury (dpeaa)DE-He213 Mu, Ying aut Ma, Lili (orcid)0000-0002-2679-9397 aut Enthalten in Toxicological research Seoul : Soc., 2008 40(2023), 1 vom: 24. Aug., Seite 73-81 (DE-627)757130194 (DE-600)2727978-9 2234-2753 nnns volume:40 year:2023 number:1 day:24 month:08 pages:73-81 https://dx.doi.org/10.1007/s43188-023-00205-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 40 2023 1 24 08 73-81 |
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10.1007/s43188-023-00205-0 doi (DE-627)SPR054377919 (SPR)s43188-023-00205-0-e DE-627 ger DE-627 rakwb eng Tian, Jie verfasserin aut Chemerin/CMKLR1 pathway exacerbates cisplatin-induced spiral ganglion neuron injury 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) under exclusive licence to Korean Society of Toxicology 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract This study investigated whether chemerin/chemokine-like receptor 1 (CMKLR1) pathway participate in cisplatin‐induced spiral ganglion neuron (SGN) damage. Middle cochlear turn was collected from C57BL/6 mice and the SGNs were cultured. Cisplatin, 2-(anaphthoyl) ethyltrimethylammonium iodide (α-NETA), or recombinant mouse chemerin was added into the medium for the treatment. Relative mRNA and protein expression was determined by RT-PCR, ELISA and Western blot, respectively. In cultured mouse cochlear SGNs, the treatment of cisplatin enhanced the secretion of chemerin and CMKLR1. Recombinant chemerin promoted but α-NETA inhibited chemerin/CMKLR1 pathway in cisplatin stimulated SGNs. Cisplatin-induced apoptosis and inflammation response in SGNs were enhanced by recombinant chemerin while inhibited by α-NETA. Recombinant chemerin promoted but α-NETA inhibited NF-κB signal in cisplatin stimulated SGNs. In conclusion, chemerin/CMKLR1 pathway regulated apoptosis and inflammation response in cisplatin-induced SGN injury through NF-κB signaling pathway. Chemerin (dpeaa)DE-He213 CMKLR1 (dpeaa)DE-He213 Cisplatin (dpeaa)DE-He213 Spiral ganglion neuron (dpeaa)DE-He213 Injury (dpeaa)DE-He213 Mu, Ying aut Ma, Lili (orcid)0000-0002-2679-9397 aut Enthalten in Toxicological research Seoul : Soc., 2008 40(2023), 1 vom: 24. Aug., Seite 73-81 (DE-627)757130194 (DE-600)2727978-9 2234-2753 nnns volume:40 year:2023 number:1 day:24 month:08 pages:73-81 https://dx.doi.org/10.1007/s43188-023-00205-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 40 2023 1 24 08 73-81 |
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10.1007/s43188-023-00205-0 doi (DE-627)SPR054377919 (SPR)s43188-023-00205-0-e DE-627 ger DE-627 rakwb eng Tian, Jie verfasserin aut Chemerin/CMKLR1 pathway exacerbates cisplatin-induced spiral ganglion neuron injury 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) under exclusive licence to Korean Society of Toxicology 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract This study investigated whether chemerin/chemokine-like receptor 1 (CMKLR1) pathway participate in cisplatin‐induced spiral ganglion neuron (SGN) damage. Middle cochlear turn was collected from C57BL/6 mice and the SGNs were cultured. Cisplatin, 2-(anaphthoyl) ethyltrimethylammonium iodide (α-NETA), or recombinant mouse chemerin was added into the medium for the treatment. Relative mRNA and protein expression was determined by RT-PCR, ELISA and Western blot, respectively. In cultured mouse cochlear SGNs, the treatment of cisplatin enhanced the secretion of chemerin and CMKLR1. Recombinant chemerin promoted but α-NETA inhibited chemerin/CMKLR1 pathway in cisplatin stimulated SGNs. Cisplatin-induced apoptosis and inflammation response in SGNs were enhanced by recombinant chemerin while inhibited by α-NETA. Recombinant chemerin promoted but α-NETA inhibited NF-κB signal in cisplatin stimulated SGNs. In conclusion, chemerin/CMKLR1 pathway regulated apoptosis and inflammation response in cisplatin-induced SGN injury through NF-κB signaling pathway. Chemerin (dpeaa)DE-He213 CMKLR1 (dpeaa)DE-He213 Cisplatin (dpeaa)DE-He213 Spiral ganglion neuron (dpeaa)DE-He213 Injury (dpeaa)DE-He213 Mu, Ying aut Ma, Lili (orcid)0000-0002-2679-9397 aut Enthalten in Toxicological research Seoul : Soc., 2008 40(2023), 1 vom: 24. Aug., Seite 73-81 (DE-627)757130194 (DE-600)2727978-9 2234-2753 nnns volume:40 year:2023 number:1 day:24 month:08 pages:73-81 https://dx.doi.org/10.1007/s43188-023-00205-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 40 2023 1 24 08 73-81 |
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10.1007/s43188-023-00205-0 doi (DE-627)SPR054377919 (SPR)s43188-023-00205-0-e DE-627 ger DE-627 rakwb eng Tian, Jie verfasserin aut Chemerin/CMKLR1 pathway exacerbates cisplatin-induced spiral ganglion neuron injury 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) under exclusive licence to Korean Society of Toxicology 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract This study investigated whether chemerin/chemokine-like receptor 1 (CMKLR1) pathway participate in cisplatin‐induced spiral ganglion neuron (SGN) damage. Middle cochlear turn was collected from C57BL/6 mice and the SGNs were cultured. Cisplatin, 2-(anaphthoyl) ethyltrimethylammonium iodide (α-NETA), or recombinant mouse chemerin was added into the medium for the treatment. Relative mRNA and protein expression was determined by RT-PCR, ELISA and Western blot, respectively. In cultured mouse cochlear SGNs, the treatment of cisplatin enhanced the secretion of chemerin and CMKLR1. Recombinant chemerin promoted but α-NETA inhibited chemerin/CMKLR1 pathway in cisplatin stimulated SGNs. Cisplatin-induced apoptosis and inflammation response in SGNs were enhanced by recombinant chemerin while inhibited by α-NETA. Recombinant chemerin promoted but α-NETA inhibited NF-κB signal in cisplatin stimulated SGNs. In conclusion, chemerin/CMKLR1 pathway regulated apoptosis and inflammation response in cisplatin-induced SGN injury through NF-κB signaling pathway. Chemerin (dpeaa)DE-He213 CMKLR1 (dpeaa)DE-He213 Cisplatin (dpeaa)DE-He213 Spiral ganglion neuron (dpeaa)DE-He213 Injury (dpeaa)DE-He213 Mu, Ying aut Ma, Lili (orcid)0000-0002-2679-9397 aut Enthalten in Toxicological research Seoul : Soc., 2008 40(2023), 1 vom: 24. Aug., Seite 73-81 (DE-627)757130194 (DE-600)2727978-9 2234-2753 nnns volume:40 year:2023 number:1 day:24 month:08 pages:73-81 https://dx.doi.org/10.1007/s43188-023-00205-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 40 2023 1 24 08 73-81 |
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Enthalten in Toxicological research 40(2023), 1 vom: 24. Aug., Seite 73-81 volume:40 year:2023 number:1 day:24 month:08 pages:73-81 |
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Enthalten in Toxicological research 40(2023), 1 vom: 24. Aug., Seite 73-81 volume:40 year:2023 number:1 day:24 month:08 pages:73-81 |
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Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract This study investigated whether chemerin/chemokine-like receptor 1 (CMKLR1) pathway participate in cisplatin‐induced spiral ganglion neuron (SGN) damage. Middle cochlear turn was collected from C57BL/6 mice and the SGNs were cultured. Cisplatin, 2-(anaphthoyl) ethyltrimethylammonium iodide (α-NETA), or recombinant mouse chemerin was added into the medium for the treatment. Relative mRNA and protein expression was determined by RT-PCR, ELISA and Western blot, respectively. 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Chemerin/CMKLR1 pathway exacerbates cisplatin-induced spiral ganglion neuron injury Chemerin (dpeaa)DE-He213 CMKLR1 (dpeaa)DE-He213 Cisplatin (dpeaa)DE-He213 Spiral ganglion neuron (dpeaa)DE-He213 Injury (dpeaa)DE-He213 |
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chemerin/cmklr1 pathway exacerbates cisplatin-induced spiral ganglion neuron injury |
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Chemerin/CMKLR1 pathway exacerbates cisplatin-induced spiral ganglion neuron injury |
| abstract |
Abstract This study investigated whether chemerin/chemokine-like receptor 1 (CMKLR1) pathway participate in cisplatin‐induced spiral ganglion neuron (SGN) damage. Middle cochlear turn was collected from C57BL/6 mice and the SGNs were cultured. Cisplatin, 2-(anaphthoyl) ethyltrimethylammonium iodide (α-NETA), or recombinant mouse chemerin was added into the medium for the treatment. Relative mRNA and protein expression was determined by RT-PCR, ELISA and Western blot, respectively. In cultured mouse cochlear SGNs, the treatment of cisplatin enhanced the secretion of chemerin and CMKLR1. Recombinant chemerin promoted but α-NETA inhibited chemerin/CMKLR1 pathway in cisplatin stimulated SGNs. Cisplatin-induced apoptosis and inflammation response in SGNs were enhanced by recombinant chemerin while inhibited by α-NETA. Recombinant chemerin promoted but α-NETA inhibited NF-κB signal in cisplatin stimulated SGNs. In conclusion, chemerin/CMKLR1 pathway regulated apoptosis and inflammation response in cisplatin-induced SGN injury through NF-κB signaling pathway. © The Author(s) under exclusive licence to Korean Society of Toxicology 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
| abstractGer |
Abstract This study investigated whether chemerin/chemokine-like receptor 1 (CMKLR1) pathway participate in cisplatin‐induced spiral ganglion neuron (SGN) damage. Middle cochlear turn was collected from C57BL/6 mice and the SGNs were cultured. Cisplatin, 2-(anaphthoyl) ethyltrimethylammonium iodide (α-NETA), or recombinant mouse chemerin was added into the medium for the treatment. Relative mRNA and protein expression was determined by RT-PCR, ELISA and Western blot, respectively. In cultured mouse cochlear SGNs, the treatment of cisplatin enhanced the secretion of chemerin and CMKLR1. Recombinant chemerin promoted but α-NETA inhibited chemerin/CMKLR1 pathway in cisplatin stimulated SGNs. Cisplatin-induced apoptosis and inflammation response in SGNs were enhanced by recombinant chemerin while inhibited by α-NETA. Recombinant chemerin promoted but α-NETA inhibited NF-κB signal in cisplatin stimulated SGNs. In conclusion, chemerin/CMKLR1 pathway regulated apoptosis and inflammation response in cisplatin-induced SGN injury through NF-κB signaling pathway. © The Author(s) under exclusive licence to Korean Society of Toxicology 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
| abstract_unstemmed |
Abstract This study investigated whether chemerin/chemokine-like receptor 1 (CMKLR1) pathway participate in cisplatin‐induced spiral ganglion neuron (SGN) damage. Middle cochlear turn was collected from C57BL/6 mice and the SGNs were cultured. Cisplatin, 2-(anaphthoyl) ethyltrimethylammonium iodide (α-NETA), or recombinant mouse chemerin was added into the medium for the treatment. Relative mRNA and protein expression was determined by RT-PCR, ELISA and Western blot, respectively. In cultured mouse cochlear SGNs, the treatment of cisplatin enhanced the secretion of chemerin and CMKLR1. Recombinant chemerin promoted but α-NETA inhibited chemerin/CMKLR1 pathway in cisplatin stimulated SGNs. Cisplatin-induced apoptosis and inflammation response in SGNs were enhanced by recombinant chemerin while inhibited by α-NETA. Recombinant chemerin promoted but α-NETA inhibited NF-κB signal in cisplatin stimulated SGNs. In conclusion, chemerin/CMKLR1 pathway regulated apoptosis and inflammation response in cisplatin-induced SGN injury through NF-κB signaling pathway. © The Author(s) under exclusive licence to Korean Society of Toxicology 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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Chemerin/CMKLR1 pathway exacerbates cisplatin-induced spiral ganglion neuron injury |
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https://dx.doi.org/10.1007/s43188-023-00205-0 |
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Mu, Ying Ma, Lili |
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10.1007/s43188-023-00205-0 |
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2024-07-04T01:19:20.891Z |
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| score |
7.3996468 |