Advantages of Creating a Model of MNU-Induced Zebrafish Retinal Degeneration

Primary loss of photoreceptors can cause varying degrees of visual impairment, eventually leading to vision loss. Age-related macular degeneration (AMD) and retinitis pigmentosa (RP) are typical examples of such retinal degenerative diseases. To determine the underlying pathological mechanism, different animal models have been developed, and MNU-induced retinal degeneration and regeneration in living animals is one of the preclinical pharmacological models. In these living animals, the zebrafish retina continues to proliferate after severe injury, and this regenerative mechanism allows the identification of cells and pathways with regenerative potential and allows the study of differences between zebrafish and other species without this regeneration. This makes MNU-induced retinal degeneration in zebrafish an increasingly popular model system that is expected to contribute to deciphering the specific molecular pathways involved in rod and cone regeneration.

Fig. 1. H&E staining of zebrafish retinas at baseline and after MNU exposure. (Tappeiner C, et al., 2013)

Service Overview

The photoreceptor-specific toxin N-methyl-N-nitrosourea (MNU) has been used extensively by our researchers in rodents to pharmacologically induce retinal degeneration. In order to meet the needs of different studies, we have also established the MNU-induced retinal degeneration model in zebrafish. This is another popular model system for your research into retinal degenerative diseases. This model is similar to the MNU-induced rodent retinal degeneration model and is primarily used to explore anti-retinal degenerative and anti-vascular therapies for the treatment of age-related macular degeneration (AMD) and retinitis pigmentosa (RP).

Explore Ace Therapeutics' Zebrafish Models of MNU-Induced Retinal Degeneration and Regeneration

Ace Therapeutics' MNU-induced zebrafish retinal degeneration and regeneration model was obtained by incubating adult zebrafish in MNU-containing water for 60 minutes at room temperature, followed by a quick freshwater rinse and placing the zebrafish in a new tank without MNU. The follow-up period was up to 30 days.

Model characteristics: Zebrafish treated with MNU showed complete retinal morphological degeneration and regeneration, including reduction of rod cells (decrease starting at day 3 with a minimal at day 8), apoptosis of rod photoreceptors, retinal inner layer regeneration (hyperplasia begins on day 3 with a maximum on day 5), and cells in the outer nuclear layer of the retina proliferate.

Available Support Services

In order to accurately judge the modeling endpoint, verify the reliability of the model, and evaluate the efficacy of potential compounds, Ace Therapeutics monitors and judges through the following methods throughout the process of model construction and pharmacological research, including but not limited to:

• Histopathology
• Quantification of TUNEL-positive cells
• Outer retinal layer (ONL) thickness
• Inner retinal layer (INL) thickness
• Electroretinogram (ERG)
• Optical coherence tomography (OCT)
• Vision assessment
• Western blot analysis
• Immunohistochemistry

Ace Therapeutics aims to provide our customers with a versatile tool to study photoreceptor-specific degeneration and understand retinal regeneration processes. In addition, we also provide solutions for the pharmacodynamic evaluation of ophthalmic products or new therapies. If you are interested in our services or need more detailed information, please feel free to contact us. Our experienced scientists are ready to help you!

References

1. Maurer E, Tschopp M, Tappeiner C, et al. Methylnitrosourea (MNU)-induced retinal degeneration and regeneration in the zebrafish: histological and functional characteristics. J Vis Exp. 2014, (92):e51909.
2. Tappeiner C, Balmer J, Iglicki M, et al. Characteristics of rod regeneration in a novel zebrafish retinal degeneration model using N-methyl-N-nitrosourea (MNU). PLoS One. 2013, 8(8):e71064.

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