Investigative Ophthalmology & Visual Science Cover Image for Volume 65, Issue 7
June 2024
Volume 65, Issue 7
Open Access
ARVO Annual Meeting Abstract  |   June 2024
Dysregulation of Nrxn1 in Early Diabetic Retinal Disease
Author Affiliations & Notes
  • Eda Kusan Unlu
    Ophthalmology, Johns Hopkins Medicine Wilmer Eye Institute, Baltimore, Maryland, United States
  • Ruth Marx-Rattner
    Ophthalmology, Johns Hopkins Medicine Wilmer Eye Institute, Baltimore, Maryland, United States
  • Kaitlyn Clark
    Ophthalmology, Johns Hopkins Medicine Wilmer Eye Institute, Baltimore, Maryland, United States
  • Valina L Dawson
    Johns Hopkins University Institute for Cell Engineering, Baltimore, Maryland, United States
  • Ted M Dawson
    Johns Hopkins University Institute for Cell Engineering, Baltimore, Maryland, United States
  • Mira Menon Sachdeva
    Ophthalmology, Johns Hopkins Medicine Wilmer Eye Institute, Baltimore, Maryland, United States
  • Footnotes
    Commercial Relationships   Eda Kusan Unlu None; Ruth Marx-Rattner None; Kaitlyn Clark None; Valina Dawson None; Ted Dawson None; Mira Sachdeva None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science June 2024, Vol.65, 878. doi:
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      Eda Kusan Unlu, Ruth Marx-Rattner, Kaitlyn Clark, Valina L Dawson, Ted M Dawson, Mira Menon Sachdeva; Dysregulation of Nrxn1 in Early Diabetic Retinal Disease. Invest. Ophthalmol. Vis. Sci. 2024;65(7):878.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose : Inner retinal dysfunction and thinning are features of early diabetic retinal disease (DRD), preceding the clinical diagnosis of diabetic retinopathy (DR). The underlying molecular mechanisms remain unclear. Recently, decreased levels of the synaptic proteins neurexins (Nrxns) have been described in the brain of a mouse model of diabetes but little is known about the role of Nrxns in the retina. The purpose of this study is to define a potential role of neurexin 1 (Nrxn1) in early diabetic retinal dysfunction. We hypothesize that Nrxn1 dysregulation occurs in the inner retina during the early phases of DRD.

Methods : Intraperitoneal injection of 60mg/kg streptozotocin (STZ) or vehicle was administered daily for five days to 8-10 week old male C57BL/6J mice, and those with blood glucose > 250 mg/dL were considered to have diabetes. Optical coherence tomography (OCT), electroretinography (ERG), and fluoresecein angiography were performed at 6 weeks after induction of diabetes. At this timepoint, retinal tissues were collected and analyzed for Nrxn1 protein expression by Western blot. Cell-type-localization and transcript expression was assessed using RNAscope in situ hybridization.

Results : Six weeks after STZ treatment, diabetic mice exhibited functional deficits on ERG and inner retinal thinning on OCT. Importantly, these alterations were noted in the absence of vascular leakage, recapitulating the neurodegenerative features of early DRD. Nrxn1 protein expression was significantly decreased in the diabetic retina. RNAscope in situ analyses revealed that neurexin transcripts are predominantly expressed in the inner retina, including in the retinal ganglion cells (RGCs). Furthermore, RGCs in the peripheral retina of diabetic mice expressed decreased Nrxn1 transcript compared with controls.

Conclusions : Our results confirm that at 6 weeks after diabetes induction, STZ-treated mice exhibit the neurodegenerative features of early DRD in the absence of vascular leakage. Decreased Nrxn1 expression in the inner retina, namely RGCs, may contribute to the phenotype of early DRD.

This abstract was presented at the 2024 ARVO Annual Meeting, held in Seattle, WA, May 5-9, 2024.

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