scholarly journals Down-regulation of AMPK signaling pathway rescues hearing loss in TFB1 transgenic mice and delays age-related hearing loss

Aging ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 5590-5611
Author(s):  
Jingjing Zhao ◽  
Gen Li ◽  
Xuan Zhao ◽  
Xin Lin ◽  
Yunge Gao ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Transgenic Mice ◽  
Signaling Pathway ◽  
Down Regulation ◽  
Ampk Signaling ◽  
Age Related ◽  
Age Related Hearing Loss

scholarly journals LncRNA AW112010 Promotes Mitochondrial Biogenesis and Hair Cell Survival: Implications for Age-Related Hearing Loss

2019 ◽  
Vol 2019 ◽  
pp. 1-13 ◽  
Author(s):  
Zhongwu Su ◽  
Hao Xiong ◽  
Jiaqi Pang ◽  
Hanqing Lin ◽  
Lan Lai ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Cell Survival ◽  
Mitochondrial Biogenesis ◽  
Noncoding Rna ◽  
Ros Generation ◽  
Aged Mouse ◽  
Ampk Signaling ◽  
Atp Assay ◽  
Age Related ◽  
Age Related Hearing Loss

Long noncoding RNA (lncRNA) disorder has been found in many kinds of age-associated diseases. However, the role of lncRNA in the development of age-related hearing loss (AHL) is still largely unknown. This study sought to uncover AHL-associated lncRNAs and the function. RNA-sequencing was conducted to profile lncRNA expression in the cochlea of an early-onset AHL mouse model. RT-qPCR assay was used to validate the expression pattern of lncRNAs. ATP assay, JC-1 assay, mitochondrial probe staining, CCK-8 assay, Western blot, and immunocytochemistry were performed to detect the effects of lncRNA AW112010 in HEI-OC1 cells and the mouse cochlea. We identified 88 significantly upregulated lncRNAs and 46 significantly downregulated lncRNAs in the cochlea of aged C57BL/6 mice. We focused on the significantly upregulated AW112010. Silencing of AW112010 decreased the ATP level, mitochondrial membrane potential, and cell viability and increased mitochondrial ROS generation under oxidative stress in HEI-OC1 cells. AW112010 overexpression promoted cell survival in HEI-OC1 cells. AW112010 knockdown reduced mitochondrial mass and impaired mitochondrial biogenesis in HEI-OC1 cells. Activation of mitochondrial biogenesis by resveratrol and STR1720 promoted cell survival. The mitochondrial biogenesis process was activated in the cochlea of aged mice. Moreover, AW112010 regulated AMPK signaling in HEI-OC1 cells. Transcription factor Arid5b elevated in the aged cochlea and induced AW112010 expression and mitochondrial biogenesis in HEI-OC1 cells. Taken together, lncRNAs are dysregulated with aging in the cochlea of C57BL/6 mice. The Arid5b/AW112010 signaling was induced in the aged mouse cochlea and positively modulated the mitochondrial biogenesis to maintain mitochondrial function.

Deterioration of the Medial Olivocochlear Efferent System Accelerates Age-Related Hearing Loss in Pax2-Isl1 Transgenic Mice

2015 ◽  
Vol 53 (4) ◽  
pp. 2368-2383 ◽  
Author(s):  
Tetyana Chumak ◽  
Romana Bohuslavova ◽  
Iva Macova ◽  
Nicole Dodd ◽  
Daniela Buckiova ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Transgenic Mice ◽  
Efferent System ◽  
Age Related ◽  
Medial Olivocochlear ◽  
Medial Olivocochlear Efferent System ◽  
Age Related Hearing Loss

scholarly journals Cre-dependent optogenetic transgenic mice without early age-related hearing loss

2018 ◽  
Author(s):  
Daniel Lyngholm ◽  
Shuzo Sakata
Keyword(s):  
Hearing Loss ◽  
Transgenic Mice ◽  
Genetic Defect ◽  
F1 Hybrids ◽  
Early Age ◽  
F1 Hybrid ◽  
Hearing Research ◽  
Brain Functions ◽  
Age Related ◽  
Age Related Hearing Loss

AbstractWith the advent of recent genetic technologies for mice, it is now feasible to investigate the circuit mechanisms of brain functions in an unprecedented manner. Although transgenic mice are commonly used on C57BL/6J (C57) background, hearing research has typically relied on different genetic backgrounds, such as CBA/Ca or CBA due to the genetic defect of C57 mice for early age-related hearing loss. This limits the utilization of available genetic resources for hearing research. Here we report congenic (>F10) Cre-dependent channelrhodopsin2 (ChR2) mice on CBA/Ca background. By crossing this line with Cre-driver mice on C57 background, F1 hybrids restored the hearing deficit of C57 mice. We also found a linear relationship between aging and hearing loss, with progression rates varied depending on genetic backgrounds (3.39 dB/month for C57; 0.82 dB/month for F1 hybrid). We further demonstrate that this approach allows to express ChR2 in a specific type of inhibitory neurons in the auditory cortex and that they can be identified within a simultaneously recorded population of neurons in awake mice. Thus, our Cre-dependent optogenetic transgenic mice on CBA/Ca background are a valuable tool to investigate the circuit mechanisms of hearing across lifespan.

RETRACTED: miR-34a/Bcl-2 signaling pathway contributes to age-related hearing loss by modulating hair cell apoptosis

2017 ◽  
Vol 661 ◽  
pp. 51-56 ◽  
Author(s):  
Qiuhong Huang ◽  
Yiqing Zheng ◽  
Yongkang Ou ◽  
Hao Xiong ◽  
Haidi Yang ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Age Related ◽  
Age Related Hearing Loss
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