Loss of retinal ganglion cells in a new genetic mouse model for primary open‐angle glaucoma

• Published in: Journal of cellular and molecular medicine 2019-08, Vol.23 (8), p.5497-5507
• Main Authors: Reinehr, Sabrina, Koch, Dennis, Weiss, Maximilian, Froemel, Franziska, Voss, Christina, Dick, H. Burkhard, Fuchshofer, Rudolf, Joachim, Stephanie C.
• Format: Article
• Language: English
• Subjects: Animal models; Animals; Antibodies; Blindness; Caspase-3; Connective tissue growth factor; Disease Models, Animal; Down-Regulation - physiology; electroretinogram; Electroretinography - methods; Female; Glaucoma; Glaucoma, Open-Angle - metabolism; Glaucoma, Open-Angle - pathology; Glial Fibrillary Acidic Protein - metabolism; Glutamate-ammonia ligase; Glutamine; Immunoglobulins; Intraocular pressure; Male; Mice; mRNA; Original; Photoreceptors; primary open‐angle glaucoma; Recoverin; Retina; Retina - metabolism; Retina - pathology; Retinal ganglion cells; Retinal Ganglion Cells - metabolism; Retinal Ganglion Cells - pathology; Rhodopsin; Risk factors; RNA, Messenger - metabolism; Software; Studies; βB1‐CTGF
• ISSN: 1582-1838; 1582-4934; 1582-4934
• DOI: 10.1111/jcmm.14433

Primary open‐angle glaucoma (POAG) is one of the most common causes for blindness worldwide. Although an elevated intraocular pressure (IOP) is the main risk factor, the exact pathology remained indistinguishable. Therefore, it is necessary to have appropriate models to investigate these mechanisms. Here, we analysed a transgenic glaucoma mouse model (βB1‐CTGF) to elucidate new possible mechanisms of the disease. Therefore, IOP was measured in βB1‐CTGF and wildtype mice at 5, 10 and 15 weeks of age. At 5 and 10 weeks, the IOP in both groups were comparable (P > 0.05). After 15 weeks, a significant elevated IOP was measured in βB1‐CTGF mice (P