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Hypoxic–ischemic injury causes functional and structural neurovascular degeneration in the juvenile mouse retina

Ischemic stroke is a major cause of long-term disabilities, including vision loss. Neuronal and blood vessel maturation can affect the susceptibility of and outcome after ischemic stroke. Although we recently reported that exposure of neonatal mice to hypoxia–ischemia (HI) severely compromises the i...

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Bibliographic Details
Published in:Scientific reports 2021-06, Vol.11 (1), p.12670-12670, Article 12670
Main Authors: Zaitoun, Ismail S., Shahi, Pawan K., Suscha, Andrew, Chan, Kore, McLellan, Gillian J., Pattnaik, Bikash R., Sorenson, Christine M., Sheibani, Nader
Format: Article
Language:English
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Summary:Ischemic stroke is a major cause of long-term disabilities, including vision loss. Neuronal and blood vessel maturation can affect the susceptibility of and outcome after ischemic stroke. Although we recently reported that exposure of neonatal mice to hypoxia–ischemia (HI) severely compromises the integrity of the retinal neurovasculature, it is not known whether juvenile mice are similarly impacted. Here we examined the effect of HI injury in juvenile mice on retinal structure and function, in particular the susceptibility of retinal neurons and blood vessels to HI damage. Our studies demonstrated that the retina suffered from functional and structural injuries, including reduced b-wave, thinning of the inner retinal layers, macroglial remodeling, and deterioration of the vasculature. The degeneration of the retinal vasculature associated with HI resulted in a significant decrease in the numbers of pericytes and endothelial cells as well as an increase in capillary loss. Taken together, these findings suggest a need for juveniles suffering from ischemic stroke to be monitored for changes in retinal functional and structural integrity. Thus, there is an emergent need for developing therapeutic approaches to prevent and reverse retinal neurovascular dysfunction with exposure to ischemic stroke.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-021-90447-5