ArticleJournal of the Association for Research in Otolaryngology : JARO2014
Cochlin in normal middle ear and abnormal middle ear deposits in DFNA9 and Coch (G88E/G88E) mice.
Article in Journal of the Association for Research in Otolaryngology : JARO, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- A systematic review of hearing and vestibular function in carriers of the Pro51Ser mutation in the COCH gene.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2019Pooled it
- Loss ofMatrix biology plus · 2025Article
- Secretion of cochlin-tomoprotein (LCCL) in the middle ear following acute tympanic injury: implications for perilymph fistula diagnosis.Frontiers in neurology · 2025Article
- Loss ofbioRxiv : the preprint server for biology · 2024Article
- Hearing loss and its association with the proteome of perilymph, cerebrospinal fluid, and tumor tissue in patients with vestibular schwannoma.Scientific reports · 2024Article
- A NovelLife (Basel, Switzerland) · 2023Article
- Adipocyte Glucocorticoid Receptor Inhibits Immune Regulatory Genes to Maintain Immune Cell Homeostasis in Adipose Tissue.Endocrinology · 2023Article
- Defining the spatial-molecular map of fibrotic tendon healing and the drivers of Scleraxis-lineage cell fate and function.Cell reports · 2022Article
- Article
- Cochlin Deficiency Protects Aged Mice from Noise-Induced Hearing Loss.International journal of molecular sciences · 2021Article
- Cochlin Deficiency Protects Against Noise-Induced Hearing Loss.Frontiers in molecular neuroscience · 2021Article
- Novel loss-of-function mutations in COCH cause autosomal recessive nonsyndromic hearing loss.Human genetics · 2020Article
- Immunohistochemical techniques for the human inner ear.Histochemistry and cell biology · 2016Review
- Histopathology of the Human Inner Ear in the p.L114P COCH Mutation (DFNA9).Audiology & neuro-otology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
DFNA9 sensorineural hearing loss and vestibular disorder, caused by mutations in COCH, has a unique identifying histopathology including prominent acellular deposits in cochlear and vestibular labyrinths. A recent study has shown presence of deposits also in middle ear structures of DFNA9-affected individuals (McCall et al., J Assoc Res Otolaryngol 12:141-149, 2004). To investigate the possible role of cochlin in the middle ear and in relation to aggregate formation, we evaluated middle ear histopathology in our Coch knock-in (Coch (G88E/G88E) ) mouse model, which harbors one of the DFNA9-causative mutations. Our findings reveal accumulation of acellular deposits in the incudomalleal and incudostapedial joints in Coch (G88E/G88E) mice, similar to those found in human DFNA9-affected temporal bones. Aggregates are absent in negative control Coch (+/+) and Coch (-/-) mice. Thickening of the tympanic membrane (TM) found in humans with DFNA9 was not appreciably detected in Coch (G88E/G88E) mice at the evaluated age. We investigated cochlin localization first in the Coch (+/+)mouse and in normal human middle ears, and found prominent and specific cochlin staining in the incudomalleal joint, incudostapedial joint, and the pars tensa of the TM, which are the three sites where abnormal deposits are detected in DFNA9-affected middle ears. Cochlin immunostaining of Coch (G88E/G88E) and DFNA9-affected middle ears showed mutant cochlin localization within areas of aggregates. Cochlin staining was heterogeneous throughout DFNA9 middle ear deposits, which appear as unorganized and overlapping mixtures of both eosinophilic and basophilic substances. Immunostaining for type II collagen colocalized with cochlin in pars tensa of the tympanic membrane. In contrast, immunostaining for type II collagen did not overlap with cochlin in interossicular joints, where type II collagen was localized in the region of the chondrocytes, but not in the thin layer of the articular surface of the ossicles nor in the eosinophilic deposits with specific cochlin staining.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.