Down-regulation of otospiralin mRNA in response to acoustic stress in guinea pig

Caravelli, Antonella; Pianese, Luigi; Saulino, Claudio; Leva, Francesca Di; Sequino, Luigi; Cocozza, Sérgio; Marciano, Elio; Franzè, Annamaria

doi:10.1016/j.heares.2004.07.011

Cited by 4 publications

(1 citation statement)

References 27 publications

(32 reference statements)

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“…Eleven studies focusing on TTS met our inclusion criteria, as detailed in the “Methods” section (Taggart et al, ; Shizuki et al, ; Caravelli et al, ; Cho et al, ; Vlajkovic et al, ; Tahera et al, ; Ruan et al, ; Miyao et al, ; Yamashita et al, ; Matsunobu et al, ; Gratton et al, ). The studies identified 40 differentially expressed molecules in the cochlea due to TTS‐inducing noise exposure (Table ).…”

Section: Resultsmentioning

confidence: 99%

Hepatocyte nuclear factor‐4 alpha in noise‐induced cochlear neuropathy

Groth

Kao

Briët

et al. 2016

Developmental Neurobiology

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Noise-induced hearing loss (NIHL) is a problem of profound clinical significance and growing magnitude. Alarmingly, even moderate noise levels, previously assumed to cause only temporary shifts in auditory thresholds ("temporary" NIHL), are now known to cause cochlear synaptopathy and subsequent neuropathy. To uncover molecular mechanisms of this neuropathy, a network analysis of genes reported to have significantly altered expression after temporary threshold shift-inducing noise exposure was performed. The transcription factor Hepatocyte Nuclear Factor-4 alpha (HNF4α), which had not previously been studied in the context of cochlear response to noise, was identified as a hub of a top-ranking network. Hnf4α expression and localization using quantitative RT-PCR and in situ hybridization, respectively, were described in adolescent and adult mice exposed to neuropathic noise levels in adolescence. Isoforms α3 and α12 in the cochlea were also identified. At every age examined, Hnf4α mRNA expression in the cochlear apex was similar to expression in the base. Hnf4α expression was evident in select cochlear cells, including spiral ganglion neurons (SGNs) and hair cells, and was significantly upregulated from 6 to 70 weeks of age, especially in SGNs. This age-related Hnf4α upregulation was inhibited by neuropathic noise exposure in adolescence. Hnf4α silencing with shRNA transfection into auditory neuroblast cells (VOT-33) reduced cell viability, as measured with the MTT assay, suggesting that Hnf4α may be involved in SGN survival. Our results motivate future studies of HNF4α in cochlear pathophysiology, especially because HNF4α mutations and polymorphisms are associated with human diseases that may include hearing loss. © 2016 Wiley Periodicals, Inc. Develop Neurobiol 76: 1374-1386, 2016.

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Section: Resultsmentioning

confidence: 99%

Hepatocyte nuclear factor‐4 alpha in noise‐induced cochlear neuropathy

Groth

Kao

Briët

et al. 2016

Developmental Neurobiology

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Adenoviral-mediated up-regulation of Otos, a novel specific cochlear gene, decreases cisplatin-induced apoptosis of cultured spiral ligament fibrocytes via MAPK/mitochondrial pathway

et al. 2008

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Epigenetic and immune function profiles associated with posttraumatic stress disorder

Uddin

Aiello

Wildman

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

461

450

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The biologic underpinnings of posttraumatic stress disorder (PTSD) have not been fully elucidated. Previous work suggests that alterations in the immune system are characteristic of the disorder. Identifying the biologic mechanisms by which such alterations occur could provide fundamental insights into the etiology and treatment of PTSD. Here we identify specific epigenetic profiles underlying immune system changes associated with PTSD. Using blood samples (n = 100) obtained from an ongoing, prospective epidemiologic study in Detroit, the Detroit Neighborhood Health Study, we applied methylation microarrays to assay CpG sites from more than 14,000 genes among 23 PTSD-affected and 77 PTSD-unaffected individuals. We show that immune system functions are significantly overrepresented among the annotations associated with genes uniquely unmethylated among those with PTSD. We further demonstrate that genes whose methylation levels are significantly and negatively correlated with traumatic burden show a similar strong signal of immune function among the PTSD affected. The observed epigenetic variability in immune function by PTSD is corroborated using an independent biologic marker of immune response to infection, CMV-a typically latent herpesvirus whose activity was significantly higher among those with PTSD. This report of peripheral epigenomic and CMV profiles associated with mental illness suggests a biologic model of PTSD etiology in which an externally experienced traumatic event induces downstream alterations in immune function by reducing methylation levels of immune-related genes.epidemiology | methylation | cytomegalovirus | cumulative trauma | psychiatry

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Down-regulation of otospiralin mRNA in response to acoustic stress in guinea pig

Cited by 4 publications

References 27 publications

Hepatocyte nuclear factor‐4 alpha in noise‐induced cochlear neuropathy

Hepatocyte nuclear factor‐4 alpha in noise‐induced cochlear neuropathy

Adenoviral-mediated up-regulation of Otos, a novel specific cochlear gene, decreases cisplatin-induced apoptosis of cultured spiral ligament fibrocytes via MAPK/mitochondrial pathway

Epigenetic and immune function profiles associated with posttraumatic stress disorder

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