FAK mediates noise-induced loss of auditory hair cell function and survival
FAK 介导噪声引起的听毛细胞功能和存活的丧失
基本信息
- 批准号:10527266
- 负责人:
- 金额:$ 23.1万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2022
- 资助国家:美国
- 起止时间:2022-06-03 至 2024-05-31
- 项目状态:已结题
- 来源:
- 关键词:AuditoryAuditory ThresholdAuditory systemBiochemicalBlood flowCell DeathCell SurvivalCell physiologyCellsCessation of lifeDynaminEnvironmentFocal Adhesion Kinase 1Functional disorderGoalsHair CellsHealthHearingIn VitroIntegrin Signaling PathwayIntegrinsKnockout MiceLabelLabyrinthLateralLeadLoudnessLoxP-flanked alleleMammalsMeasurementMediatingMediator of activation proteinMethodsMitochondriaMolecularMolecular ConformationMorphologyMusNatural regenerationNatureNoiseNoise-Induced Hearing LossOrgan of CortiOrganellesOuter Hair CellsPathway interactionsPhosphorylationPhosphotransferasesPhysiologyPreventionProcessProductionProtein Tyrosine KinaseProteinsReactive Oxygen SpeciesRoleSensorySignal TransductionStressStretchingTestingTimeTransgenic MiceWorkbasebiological adaptation to stresscell typeenvironmental changefluorescence imaginghearing impairmenthigh resolution imagingin vivoinnovationmitochondrial dysfunctionmouse modelnew therapeutic targetnovelpreservationprogramssoundsuccess
项目摘要
Project Summary
Mitochondrial dysfunction has long been recognized as an underlying mechanism of noise-induced loss of
hearing sensitivity (NIHL). However, the initiating processes that lead to this dysfunction is poorly understood.
This proposal is founded upon new and important findings involving changes in mitochondrial dynamics in outer
hair cells after loud sound exposure. Mitochondria are highly dynamic organelles that constantly undergo fission
and fusion to adapt to changes in the cellular environment, and it is becoming increasingly clear that
mitochondrial morphology is directly related to mitochondrial function and, therefore, the health and survival of
the cell. The studies proposed here will examine a potential integrin signaling pathway for induction of
mitochondrial fission activity. Specifically, we will investigate the role of FAK as a mediator of noise-induced
overstimulation of OHCs leading to cell death and loss of hearing sensitivity.
项目概要
线粒体功能障碍长期以来被认为是噪音引起的线粒体功能丧失的潜在机制。
听力敏感性(NIHL)。然而,人们对导致这种功能障碍的起始过程知之甚少。
该提议建立在涉及外线粒体动力学变化的新的重要发现的基础上
暴露于大声声音后的毛细胞。线粒体是高度动态的细胞器,不断进行裂变
和融合以适应细胞环境的变化,而且越来越清楚的是
线粒体形态与线粒体功能直接相关,因此,线粒体的健康和生存
细胞。这里提出的研究将检查潜在的整合素信号通路,以诱导
线粒体裂变活动。具体来说,我们将研究 FAK 作为噪声诱发介质的作用
过度刺激 OHC 会导致细胞死亡和听力敏感性丧失。
项目成果
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{{ truncateString('ALFRED L NUTTALL', 18)}}的其他基金
FAK mediates noise-induced loss of auditory hair cell function and survival
FAK 介导噪声引起的听毛细胞功能和存活的丧失
- 批准号:
10634695 - 财政年份:2022
- 资助金额:
$ 23.1万 - 项目类别:
3-D optical imaging of the in vivo organ of Corti motion at a sub-nanometer scale
体内柯蒂运动器官亚纳米级 3D 光学成像
- 批准号:
7986343 - 财政年份:2009
- 资助金额:
$ 23.1万 - 项目类别:
3-D optical imaging of the in vivo organ of Corti motion at a sub-nanometer scale
体内柯蒂运动器官亚纳米级 3D 光学成像
- 批准号:
8197387 - 财政年份:2009
- 资助金额:
$ 23.1万 - 项目类别:
3-D optical imaging of the in vivo organ of Corti motion at a sub-nanometer scale
体内柯蒂运动器官亚纳米级 3D 光学成像
- 批准号:
8372239 - 财政年份:2009
- 资助金额:
$ 23.1万 - 项目类别:
Low Optical Coherence Interferometry for the Cochlea
耳蜗低光学相干干涉测量
- 批准号:
6869207 - 财政年份:2004
- 资助金额:
$ 23.1万 - 项目类别:
Low Optical Coherence Interferometry for the Cochlea
耳蜗低光学相干干涉测量
- 批准号:
6998876 - 财政年份:2004
- 资助金额:
$ 23.1万 - 项目类别:
相似海外基金
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声音和压力在内耳中相互作用导致听觉阈值变化的机制
- 批准号:
8211282 - 财政年份:1983
- 资助金额:
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Standard Grant