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Abstract #92838 Published in IGR 22-1
Activation of Apoptosis in a βB1-CTGF Transgenic Mouse Model
Weiss M; Reinehr S; Mueller-Buehl AM; Doerner JD; Fuchshofer R; Stute G; Dick HB; Joachim SCInternational journal of molecular sciences 2021; 22:
To reveal the pathomechanisms of glaucoma, a common cause of blindness, suitable animal models are needed. As previously shown, retinal ganglion cell and optic nerve degeneration occur in βB1-CTGF mice. Here, we aimed to determine possible apoptotic mechanisms and degeneration of different retinal cells. Hence, retinae were processed for immunohistology ( = 5-9/group) and quantitative real-time PCR analysis ( = 5-7/group) in 5- and 10-week-old βB1-CTGF and wildtype controls. We noted significantly more cleaved caspase 3 cells in βB1-CTGF retinae at 5 ( = 0.005) and 10 weeks ( = 0.02), and a significant upregulation of and mRNA levels ( < 0.05). Furthermore, more terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) cells were detected in transgenic mice at 5 ( = 0.03) and 10 weeks ( = 0.02). Neurofilament H staining ( = 0.01) as well as ( = 0.02) and ( = 0.009) mRNA levels were significantly decreased at 10 weeks. GABAergic synapse intensity was lower at 5 weeks, while no alterations were noted at 10 weeks. The glutamatergic synapse intensity was decreased at 5 ( = 0.007) and 10 weeks ( = 0.01). No changes were observed for bipolar cells, photoreceptors, and macroglia. We conclude that apoptotic processes and synapse loss precede neuronal death in this model. This slow progression rate makes the βB1-CTGF mice a suitable model to study primary open-angle glaucoma.
Experimental Eye Research Institute, University Eye Hospital, Ruhr-University Bochum, In der Schornau 23-25, 44892 Bochum, Germany.
Full articleClassification:
5.1 Rodent (Part of: 5 Experimental glaucoma; animal models)
