ArticleBMC veterinary research2021
A defect in the NOG gene increases susceptibility to spontaneous superficial chronic corneal epithelial defects (SCCED) in boxer dogs.
Article in BMC veterinary research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 16 citations in OpenAlex.
- Diagnostic Ophthalmology.The Canadian veterinary journal = La revue veterinaire canadienne · 2025Article
- Commercial amniotic membrane extract eye drops for canine SCCED: a retrospective clinical evaluation.Frontiers in veterinary science · 2025Article
- Four new genome sequences of the Pallas's cat (Frontiers in genetics · 2024Article
- Application of Noggin-Coated Electrospun Scaffold in Corneal Wound Healing.Translational vision science & technology · 2023Article
- Evaluation of corneal ulcer type, skull conformation, and other risk factors in dogs: A retrospective study of 347 cases.The Canadian veterinary journal = La revue veterinaire canadienne · 2023Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundSuperficial chronic corneal epithelial defects (SCCEDs) are spontaneous corneal defects in dogs that share many clinical and pathologic characteristics to recurrent corneal erosions (RCE) in humans. Boxer dogs are predisposed to SCCEDs, therefore a search for a genetic defect was performed to explain this susceptibility. DNA was extracted from blood collected from Boxer dogs with and without SCCEDs followed by whole genome sequencing (WGS). RNA sequencing of corneal tissue and immunostaining of corneal sections from affected SCCED Boxer dogs with a deletion in the NOG gene and affected non-Boxer dogs without the deletion were performed.
resultsA 30 base pair deletion at a splice site in Noggin (NOG) (Chr 9:31453999) was identified by WGS and was significantly associated (P < 0.0001) with Boxer SCCEDs compared to unaffected non-Boxer dogs. NOG, BMP4, MMP13, and NCAM1 all had significant fold reductions in expression and SHH was significantly increased in Boxers with the NOG deletion as identified by RNA-Seq. Corneal IHC from NOG deletion dogs with SCCEDs had lower NOG and significantly higher scores of BMP2.
conclusionsMany Boxer dogs with SCCED have a genetic defect in NOG. NOG is a constitutive protein in the cornea which is a potent inhibitor of BMP, which likely regulate limbal epithelial progenitor cells (LEPC). Dysregulation of LEPC may play a role in the pathogenesis of RCE.
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