ArticleHistochemistry and cell biology2007
OPA1, the disease gene for optic atrophy type Kjer, is expressed in the inner ear.
Article in Histochemistry and cell biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Distinct genetic patterns and natural history of OPA1-related auditory neuropathy in Chinese population.Orphanet journal of rare diseases · 2025Article
- The human OPA1Cellular and molecular life sciences : CMLS · 2024Article
- Mitochondrial DNA damage triggers spread of Parkinson's disease-like pathology.Molecular psychiatry · 2023Article
- Article
- Cochlear Implantation Outcomes in Patients with Auditory Neuropathy Spectrum Disorder of Genetic and Non-Genetic Etiologies: A Multicenter Study.Biomedicines · 2022Article
- Opa1 Prevents Apoptosis and Cisplatin-Induced Ototoxicity in Murine Cochleae.Frontiers in cell and developmental biology · 2021Article
- Auditory Neuropathy as the Initial Phenotype for Patients WithFrontiers in cell and developmental biology · 2021Article
- ATP1A3 mutations can cause progressive auditory neuropathy: a new gene of auditory synaptopathy.Scientific reports · 2017Article
- Distributed abnormalities of brain white matter architecture in patients with dominant optic atrophy and OPA1 mutations.Journal of neurology · 2015Article
- OPA1-related auditory neuropathy: site of lesion and outcome of cochlear implantation.Brain : a journal of neurology · 2015Article
- State-of-the-art technologies, current opinions and developments, and novel findings: news from the field of histochemistry and cell biology.Histochemistry and cell biology · 2008Review
- Recent progress in histochemistry.Histochemistry and cell biology · 2007Review
- The neuro-ophthalmology of mitochondrial disease.Survey of ophthalmologyReview
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autosomal dominant optic atrophy (adOA) is the most common form of hereditary optic neuropathy. The majority of cases are associated with mutations in the OPA1 gene. A few cases of adOA are known to be associated with moderate progressive hearing loss. To gain insight into the pathogenesis of this hearing loss, we performed expression analyses of OPA1 in the rat auditory and vestibular organ. In cochlear tissue, several splice variants of OPA1 were detected, which are also expressed in retinal tissue. OPA1 mRNA and protein was found in the hair cells and ganglion cells of the cochlea and vestibular organ. In ganglion cells, OPA1 mRNA and protein was already detectable at birth, whereas in the organ of Corti OPA1 mRNA and protein was up-regulated after birth and reached mature-like expression level during the onset of hearing. Comparison of an antibody directed to the mitochondrial marker protein HSP60 with antibodies directed to different amino acid stretches of OPA1 revealed a sub-cellular distribution of OPA1 in areas of significant density of mitochondria. The data suggest that defects in OPA1 cause hearing disorders due to a progressing metabolic disturbance of hair and ganglion cells in the inner ear.
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