ArticleHuman molecular genetics2015
A defect in early myogenesis causes Otitis media in two mouse models of 22q11.2 Deletion Syndrome.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- Auditory evoked-potential abnormalities in a mouse model of 22q11.2 Deletion Syndrome and their interactions with hearing impairment.Translational psychiatry · 2025Article
- RNA 3'end tailing safeguards cells against products of pervasive transcription termination.Nature communications · 2024Article
- Altered corollary discharge signaling in the auditory cortex of a mouse model of schizophrenia predisposition.Nature communications · 2023Article
- Increased Central Auditory Gain and Decreased Parvalbumin-Positive Cortical Interneuron Density in theBiological psychiatry global open science · 2023Article
- The interconnected relationships between middle ear bulla size, cavitation defects, and chronic otitis media revealed in a syndromic mouse model.Frontiers in genetics · 2022Article
- Differences in the Tensor Veli Palatini Muscle and Hearing Status in Children With and Without 22q11.2 Deletion Syndrome.The Cleft palate-craniofacial journal : official publication of the American Cleft Palate-Craniofacial Association · 2020Article
- Panel 3: Genomics, precision medicine and targeted therapies.International journal of pediatric otorhinolaryngology · 2020Review
- Chronic otitis media is initiated by a bulla cavitation defect in the FBXO11 mouse model.Disease models & mechanisms · 2019Article
- Current Understanding of Host Genetics of Otitis Media.Frontiers in genetics · 2019Review
- Mapping the distribution of stem/progenitor cells across the mouse middle ear during homeostasis and inflammation.Development (Cambridge, England) · 2018Article
- Major evolutionary transitions and innovations: the tympanic middle ear.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Otologic and audiologic findings in 22q11.2 deletion syndrome.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 · 2017Article
- Ectodysplasin signalling deficiency in mouse models of hypohidrotic ectodermal dysplasia leads to middle ear and nasal pathology.Human molecular genetics · 2016Article
- The development of the mammalian outer and middle ear.Journal of anatomy · 2016Review
- Innate Immunity: Orchestrating Inflammation and Resolution of Otitis Media.Current allergy and asthma reports · 2016Review
- Identification of a Novel ENU-Induced Mutation in MouseNeural plasticity · 2016Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Otitis media (OM), the inflammation of the middle ear, is the most common disease and cause for surgery in infants worldwide. Chronic Otitis media with effusion (OME) often leads to conductive hearing loss and is a common feature of a number of craniofacial syndromes, such as 22q11.2 Deletion Syndrome (22q11.2DS). OM is more common in children because the more horizontal position of the Eustachian tube (ET) in infants limits or delays clearance of middle ear effusions. Some mouse models with OM have shown alterations in the morphology and angle of the ET. Here, we present a novel mechanism in which OM is caused not by a defect in the ET itself but in the muscles that control its function. Our results show that in two mouse models of 22q11.2DS (Df1/+ and Tbx1(+/-)) presenting with bi- or unilateral OME, the fourth pharyngeal arch-derived levator veli palatini muscles were hypoplastic, which was associated with an earlier altered pattern of MyoD expression. Importantly, in mice with unilateral OME, the side with the inflammation was associated with significantly smaller muscles than the contralateral unaffected ear. Functional tests examining ET patency confirmed a reduced clearing ability in the heterozygous mice. Our findings are also of clinical relevance as targeting hypoplastic muscles might present a novel preventative measure for reducing the high rates of OM in 22q11.2DS patients.
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