ArticleBirth defects research. Part A, Clinical and molecular teratology2013
An in vitro mouse model of congenital cytomegalovirus-induced pathogenesis of the inner ear cochlea.
Article in Birth defects research. Part A, Clinical and molecular teratology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Congenital Deafness and Recent Advances Towards Restoring Hearing Loss.Current protocols · 2021Article
- Role of the Stria Vascularis in the Pathogenesis of Sensorineural Hearing Loss: A Narrative Review.Frontiers in neuroscience · 2021Review
- Mechanism and Prevention of Spiral Ganglion Neuron Degeneration in the Cochlea.Frontiers in cellular neuroscience · 2021Review
- CMV-induced embryonic mouse organ of corti dysplasia: Network architecture of dysfunctional lateral inhibition.Birth defects research. Part A, Clinical and molecular teratology · 2015Article
- Developing a Vaccine against Congenital Cytomegalovirus (CMV) Infection: What Have We Learned from Animal Models? Where Should We Go Next?Future virology · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Congenital human cytomegalovirus (CMV) infection is the leading nongenetic etiology of sensorineural hearing loss (SNHL) at birth and prelingual SNHL not expressed at birth. The paucity of temporal bone autopsy specimens from infants with congenital CMV infection has hindered the critical correlation of histopathology with pathogenesis. Here, we present an in vitro embryonic mouse model of CMV-infected cochleas that mimics the human sites of viral infection and associated pathology. There is a striking dysplasia/hyperplasia in mouse CMV-infected cochlear epithelium and mesenchyme, including organ of Corti hair and supporting cells and stria vascularis. This is concomitant with significant dysregulation of p19, p21, p27, and Pcna gene expression, as well as proliferating cell nuclear antigen (PCNA) protein expression. Other pathologies similar to those arising from known deafness gene mutations include downregulation of KCNQ1 protein expression in the stria vascularis, as well as hypoplastic and dysmorphic melanocytes. Thus, this model provides a relevant and reliable platform within which the detailed cell and molecular biology of CMV-induced deafness may be studied.
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Registered trials
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