The influence of NF-ΚB signal-transduction pathways on the murine inner ear by acoustic overstimulation
dc.contributor.author | Yamamoto, Hiroshi | en_US |
dc.contributor.author | Omelchenko, Irina | en_US |
dc.contributor.author | Shi, Xiaorui | en_US |
dc.contributor.author | Nuttall, Alfred L. | en_US |
dc.date.accessioned | 2009-05-04T18:26:44Z | |
dc.date.available | 2010-07-06T14:30:32Z | en_US |
dc.date.issued | 2009-06 | en_US |
dc.identifier.citation | Yamamoto, Hiroshi; Omelchenko, Irina; Shi, Xiaorui; Nuttall, Alfred L. (2009). "The influence of NF-ΚB signal-transduction pathways on the murine inner ear by acoustic overstimulation." Journal of Neuroscience Research 87(8): 1832-1840. <http://hdl.handle.net/2027.42/62147> | en_US |
dc.identifier.issn | 0360-4012 | en_US |
dc.identifier.issn | 1097-4547 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/62147 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=19185019&dopt=citation | en_US |
dc.description.abstract | Nuclear factor-kappa B (NF-ΚB) comprises a family of inducible transcription factors that serve as important regulators of the host immune and inflammatory responses. The NF-ΚB signals are activated via the canonical and/or noncanonical pathways in response to diverse stimuli. The excessive action of NF-ΚB signal-transduction pathways frequently causes self-injurious phenomena such as allergic diseases, vascular disorders, and ischemia–reperfusion neuronal damage. In the inner ear, the role of NF-ΚB has not been clarified because the activated NF-ΚB signals potentially induce both cytoprotective and cytotoxic target genes after ototoxic stimulation. In the present study, we investigated the response of NF-ΚB in both the canonical and noncanonical pathways to acoustic overstimulation (117 dB/SPL/2 hr) and followed the change of inflammatory factors (inducible nitric oxide synthase [iNOS], intracellular adhesion molecule-1 [ICAM-1], and vascular cell adhesion molecule-1 [VCAM-1]) in the cochlear lateral wall (CLW) and the rest of cochlea (RoC). By means of immunohistochemistry combined with confocal microscopy and reverse transcriptase–polymerase chain reaction techniques, we found the response of NF-ΚB family members (NF-ΚB1, 2, RelA, and RelB) at the transcription level. After the NF-ΚB signaling, the inflammatory factors were significantly increased in the CLW and the RoC. Additionally, at the protein level, the prominent expression of adhesion molecules (ICAM-1 and VCAM-1) was observed in the tissue around the capillaries in the stria vascularis. These results show that acoustic overstimulation causes the NF-ΚB signaling to overexpress the inflammatory factors in the inner ear, and the up-regulation of the adhesion molecules (ICAM-1 and VCAM-1) and iNOS potentially influence the hemodynamics and the cellular integrity in the stria vascularis. © 2009 Wiley-Liss, Inc. | en_US |
dc.format.extent | 313623 bytes | |
dc.format.extent | 3118 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.publisher | Wiley Subscription Services, Inc., A Wiley Company | en_US |
dc.subject.other | Life and Medical Sciences | en_US |
dc.subject.other | Neuroscience, Neurology and Psychiatry | en_US |
dc.title | The influence of NF-ΚB signal-transduction pathways on the murine inner ear by acoustic overstimulation | en_US |
dc.type | Article | en_US |
dc.rights.robots | IndexNoFollow | en_US |
dc.subject.hlbsecondlevel | Molecular, Cellular and Developmental Biology | en_US |
dc.subject.hlbsecondlevel | Neurosciences | en_US |
dc.subject.hlbsecondlevel | Psychology | en_US |
dc.subject.hlbsecondlevel | Public Health | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.subject.hlbtoplevel | Social Sciences | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Oregon Hearing Research Center, Oregon Health and Science University, Portland, Oregon ; Department of Otolaryngology, Renji Hospital, Shanghai Jiao Tong University, Shanghai, China ; Kresge Hearing Research Institute, University of Michigan, Ann Arbor, Michigan ; Oregon Health and Science University, Oregon Hearing Research Center, 3181 SW Sam Jackson Park Road, NRC04, Portland, OR 97239-3098 | en_US |
dc.contributor.affiliationother | Oregon Hearing Research Center, Oregon Health and Science University, Portland, Oregon ; Department of Otorhinolaryngology, Nagoya University School of Medicine, Nagoya, Japan | en_US |
dc.contributor.affiliationother | Oregon Hearing Research Center, Oregon Health and Science University, Portland, Oregon | en_US |
dc.contributor.affiliationother | Oregon Hearing Research Center, Oregon Health and Science University, Portland, Oregon ; Department of Otolaryngology, Renji Hospital, Shanghai Jiao Tong University, Shanghai, China | en_US |
dc.identifier.pmid | 19185019 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/62147/1/22018_ftp.pdf | |
dc.identifier.doi | 10.1002/jnr.22018 | en_US |
dc.identifier.source | Journal of Neuroscience Research | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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