Linked Life Data

21321603

Source:http://linkedlifedata.com/resource/pubmed/id/21321603

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pubmed-article:21321603pubmed:abstractTextWe herein investigated the role of the STAT signaling cascade in the production of pro-inflammatory cytokines and cisplatin ototoxicity. A significant hearing impairment caused by cisplatin injection was observed in Balb/c (wild type, WT) and STAT4(-/-), but not in STAT6(-/-) mice. Moreover, the expression levels of the protein and mRNA of pro-inflammatory cytokines, including TNF-?, IL-1?, and IL-6, were markedly increased in the serum and cochlea of WT and STAT4(-/-), but not STAT6(-/-) mice. Organotypic culture revealed that the shape of stereocilia bundles and arrays of sensory hair cell layers in the organ of Corti from STAT6(-/-) mice were intact after treatment with cisplatin, whereas those from WT and STAT4(-/-) mice were highly distorted and disarrayed after the treatment. Cisplatin induced the phosphorylation of STAT6 in HEI-OC1 auditory cells, and the knockdown of STAT6 by STAT6-specific siRNA significantly protected HEI-OC1 auditory cells from cisplatin-induced cell death and inhibited pro-inflammatory cytokine production. We further demonstrated that IL-4 and IL-13 induced by cisplatin modulated the phosphorylation of STAT6 by binding with IL-4 receptor alpha and IL-13R?1. These findings suggest that STAT6 signaling plays a pivotal role in cisplatin-mediated pro-inflammatory cytokine production and ototoxicity.lld:pubmed
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pubmed-article:21321603pubmed:year2011lld:pubmed
pubmed-article:21321603pubmed:articleTitleCisplatin ototoxicity involves cytokines and STAT6 signaling network.lld:pubmed
pubmed-article:21321603pubmed:affiliationVestibulocochlear Research Center & Department of Microbiology, Wonkwang University, Iksan, Jeonbuk 570-749, Korea.lld:pubmed
pubmed-article:21321603pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:21321603pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed