DC Field | Value | Language |
---|---|---|
dc.contributor.author | J O Lim | - |
dc.contributor.author | J W Ko | - |
dc.contributor.author | N R Shin | - |
dc.contributor.author | T Y Jung | - |
dc.contributor.author | C Moon | - |
dc.contributor.author | Hyoung-Chin Kim | - |
dc.contributor.author | I S Shin | - |
dc.contributor.author | J C Kim | - |
dc.date.accessioned | 2020-02-07T16:30:11Z | - |
dc.date.available | 2020-02-07T16:30:11Z | - |
dc.date.issued | 2019 | - |
dc.identifier.issn | 0340-5761 | - |
dc.identifier.uri | 10.1007/s00204-019-02507-5 | ko |
dc.identifier.uri | https://oak.kribb.re.kr/handle/201005/19063 | - |
dc.description.abstract | This study investigated whether protein arginine methyltransferase (PRMT) and the cannabinoid system are involved in cisplatin-induced ototoxicity. Cisplatin increased cytosine-cytosine-adenosine-adenosine-thymidine-enhancer-binding protein homologous protein expression. This effect is indicative of an increase in endoplasmic reticulum (ER) stress, and apoptosis signaling including cleavage of caspase-3, caspase-9, poly-adenosine diphosphate-ribose polymerase, and phospho-p53, as well as expression of PRMT3, PRMT4 and fatty acid amide hydrolase (FAAH)1 in House Ear Institute-Organ of Corti 1 (HEI-OC1) cells. In addition, overexpression of PRMT3 or PRMT4 increased the expression of FAAH1 expression, apoptosis, and ER stress signaling in HEI-OC1 cells, whereas PRMT3 or PRMT4 knockdown had the opposite effect. Furthermore, overexpression of FAAH1 increased apoptosis and ER stress, but expression of the PRMTs was unchanged. In addition, a cannabinoid 1 receptor agonist and FAAH inhibitor attenuated apoptosis and ER stress, while cisplatin increased the binding of PRMT3 with FAAH1. In the in vivo experiments, cisplatin was injected intraperitoneally at 6 mg/kg/day into C57BL/6 mice, and 7 days later, this study confirmed that PRMT3 and PRMT4 were upregulated in the organ of Corti of the mice. These results indicate that cisplatin-induced ototoxicity was correlated with PRMT3, PRMT4 and the cannabinoid system, and PRMT3 binding with FAAH1 was increased by cisplatin in HEI-OC1 cells. Therefore, this study suggests that PRMT3 mediates cisplatin-induced ototoxicity via interaction with FAAH1 in vitro and in vivo. | - |
dc.publisher | Springer | - |
dc.title | Cisplatin-induced ototoxicity involves interaction of PRMT3 and cannabinoid system | - |
dc.title.alternative | Cisplatin-induced ototoxicity involves interaction of PRMT3 and cannabinoid system | - |
dc.type | Article | - |
dc.citation.title | Archives of Toxicology | - |
dc.citation.number | 0 | - |
dc.citation.endPage | 2346 | - |
dc.citation.startPage | 2335 | - |
dc.citation.volume | 93 | - |
dc.contributor.affiliatedAuthor | Hyoung-Chin Kim | - |
dc.contributor.alternativeName | 임제오 | - |
dc.contributor.alternativeName | 고제원 | - |
dc.contributor.alternativeName | 신나래 | - |
dc.contributor.alternativeName | 정태양 | - |
dc.contributor.alternativeName | 문창종 | - |
dc.contributor.alternativeName | 김형진 | - |
dc.contributor.alternativeName | 신인식 | - |
dc.contributor.alternativeName | 김종춘 | - |
dc.identifier.bibliographicCitation | Archives of Toxicology, vol. 93, pp. 2335-2346 | - |
dc.identifier.doi | 10.1007/s00204-019-02507-5 | - |
dc.subject.keyword | Cannabinoid system | - |
dc.subject.keyword | Cisplatin | - |
dc.subject.keyword | Mechanism of action | - |
dc.subject.keyword | Ototoxicity | - |
dc.subject.keyword | PRMT | - |
dc.subject.local | Cannabinoid system | - |
dc.subject.local | cisplatin | - |
dc.subject.local | Cisplatin | - |
dc.subject.local | Mechanism of action | - |
dc.subject.local | Ototoxicity | - |
dc.subject.local | PRMT | - |
dc.description.journalClass | Y | - |
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