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Retinal Photoreceptor Protection in an AMD-Related Mouse Model by Selective Sigma-1 or Sigma-2 Receptor Modulation

Mavlyutov, Timur A., Li, Jing, Liu, Xinying, Shen, Hongtao, Yang, Huan, McCurdy, Christopher R., Pattnaik, Bikash, Guo, Lian-Wang·2022·Genes
DOI 10.3390/genes13122386PMC PMC9778362
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Abstract

The structurally and genetically distinct sigma-1 receptor (S1R) and sigma-2 receptor (S2R) comprise a unique class of drug binding sites. Their alleles are associated with human diseases involving neuronal systems, such as age-related macular degeneration (AMD) characterized by photoreceptor and retinal pigment epithelium (RPE) atrophy. Previous studies have suggested neuroprotective benefits for the brain and retina from pharmacological modulation of S1R and/or S2R. However, the effect of such modulation on AMD pathology remains underexplored. Here, we evaluated S1R- or S2R-selective modulation in an AMD-related model of Abca4−/−Rdh8−/− mice with a disrupted visual cycle that predisposes RPE and photoreceptors to illumination-induced damage. For S1R modulation, we used (+)-pentazocine, which is a high-affinity S1R-selective drug. For S2R modulation, we chose CM398, a high-affinity and highly S2R-selective ligand with drug-like properties. Abca4−/−Rdh8−/− mice received a single i.p. injection of (+)-pentazocine or CM398 or vehicle 30 min before illumination. Pretreatment with (+)-pentazocine improved electroretinogram a- and b-waves compared to that with vehicle. Consistently, in another AMD-related mouse model induced by tail-vein injected NaIO3, S1R genetic ablation aggravated photoreceptor loss. In Abca4−/−Rdh8−/− mice, pretreatment with CM398 appeared to partially avert illumination-induced photoreceptor loss and autofluorescent granule formation that signals RPE damage, as revealed by optical coherence tomography. Thus, this study using AMD-related models provides evidence of photoreceptor protection afforded by selective modulation of S1R or S2R.

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  • S2R expression is elevated in retinal pigment epithelium-specific Clic4 knockout mice, which exhibit functional and pathological hallmarks of dry AMD; TMEM97 knockout mice have exhibited conflicting results in dry AMD models; and S2R-selective modulation with CM398 reduced photoreceptor loss and retinal autofluorescent granules in an illumination-induced AMD model.

    “S2R expression is elevated in retinal pigment epithelium-specific Clic4 knockout mice, which exhibit both functional and pathological hallmarks of dry AMD. Conversely, TMEM97 knockout mice have exhibited conflicting results in dry AMD models, which are likely dependent upon the type of stressor used to induce pathology. Intravenous administration of sodium iodate to TMEM97 knockout animals induced”

    From Sigma-2 Receptors—From Basic Biology to Therapeutic Target: A Focus on Age-Related Degenerative Diseases (2023) · cites this paper as [84]

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Metadata

Authors
Mavlyutov, T. A., Li, J., Liu, X., Shen, H., Yang, H., McCurdy, C. R., Pattnaik, B., & Guo, L.-W.
Affiliations
  • Department of Surgery, University of Wisconsin, Madison, WI 53705, USA
  • Department of Surgery, School of Medicine, University of Virginia, Charlottesville, VA 22908, USA
  • Department of Pediatrics, University of Wisconsin, Madison, WI 53705, USA
  • Department of Medicinal Chemistry, College of Pharmacy, University of Florida, Gainesville, FL 32610, USA
ORCID
Venue
Genes
Publisher
MDPI AG
Published
2022-12-16
Volume
13
Issue
12
Pages
2386
ISSN
2073-4425
DOI
10.3390/genes13122386
PMC
PMC9778362
Cited by
7
References
4
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • NEI (EY022678, EY029809, P30EY016665)
  • the RRF-Rebecca Meyer Brown Professorship of McPherson Eye Research Institute (EY022678, EY029809, P30EY016665)
  • University of Wisconsin-Madison Vision Core (EY022678, EY029809, P30EY016665)

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