Cisplatin-induced ototoxicity involves interaction of PRMT3 and cannabinoid system

Cited 2 time in scopus
Metadata Downloads

Full metadata record

DC FieldValueLanguage
dc.contributor.authorJ O Lim-
dc.contributor.authorJ W Ko-
dc.contributor.authorN R Shin-
dc.contributor.authorT Y Jung-
dc.contributor.authorC Moon-
dc.contributor.authorHyoung-Chin Kim-
dc.contributor.authorI S Shin-
dc.contributor.authorJ C Kim-
dc.date.accessioned2020-02-07T16:30:11Z-
dc.date.available2020-02-07T16:30:11Z-
dc.date.issued2019-
dc.identifier.issn0340-5761-
dc.identifier.uri10.1007/s00204-019-02507-5ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/19063-
dc.description.abstractThis 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.publisherSpringer-
dc.titleCisplatin-induced ototoxicity involves interaction of PRMT3 and cannabinoid system-
dc.title.alternativeCisplatin-induced ototoxicity involves interaction of PRMT3 and cannabinoid system-
dc.typeArticle-
dc.citation.titleArchives of Toxicology-
dc.citation.number0-
dc.citation.endPage2346-
dc.citation.startPage2335-
dc.citation.volume93-
dc.contributor.affiliatedAuthorHyoung-Chin Kim-
dc.contributor.alternativeName임제오-
dc.contributor.alternativeName고제원-
dc.contributor.alternativeName신나래-
dc.contributor.alternativeName정태양-
dc.contributor.alternativeName문창종-
dc.contributor.alternativeName김형진-
dc.contributor.alternativeName신인식-
dc.contributor.alternativeName김종춘-
dc.identifier.bibliographicCitationArchives of Toxicology, vol. 93, pp. 2335-2346-
dc.identifier.doi10.1007/s00204-019-02507-5-
dc.subject.keywordCannabinoid system-
dc.subject.keywordCisplatin-
dc.subject.keywordMechanism of action-
dc.subject.keywordOtotoxicity-
dc.subject.keywordPRMT-
dc.subject.localCannabinoid system-
dc.subject.localcisplatin-
dc.subject.localCisplatin-
dc.subject.localMechanism of action-
dc.subject.localOtotoxicity-
dc.subject.localPRMT-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > Laboratory Animal Resource & Research Center > 1. Journal Articles
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.