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Receptor-Interacting Protein Kinase-3 Expression Impacts Ocular Vascular Development and Pathological Neovascularization

Authors :
Yong-Seok Song
Shoujian Wang
SunYoung Park
Barbara Hanna
Kelsey J. Johnson
Soesiawati R. Darjatmoko
Mohammad Ali Saghiri
Ali Mohammad Saghiri
Bo Liu
Christine M. Sorenson
Nader Sheibani
Source :
Cells, Vol 13, Iss 24, p 2109 (2024)
Publication Year :
2024
Publisher :
MDPI AG, 2024.

Abstract

Functional cell death pathways are essential for normal ocular vascular development and tissue homeostasis. As our understanding of necrosis-based cell death pathways has expanded, the inclusion of regulated forms, including necroptosis, ferroptosis, and oxytosis, has occurred. Although the existence of these pathways is well described, our understanding of their role during vascular development and pathological neovascularization is very limited. Here, we examined the role of receptor-interacting protein kinase-3 (Ripk3), a key regulator of necroptosis, in postnatal retinal vascularization and retinal and choroidal neovascularization under pathological conditions. Postnatal vascularization of the retinal superficial layer in the absence of Ripk3 (Ripk3−/−) was not significantly different from wild-type mice. However, we noted decreased retinal endothelial cells and pericyte numbers at 3 weeks of age when the formation of the retinal primary vascular plexus was complete. In contrast, choroidal and retinal neovascularization following laser treatment and oxygen-induced ischemic retinopathy increased in the absence of Ripk3 expression, respectively. In addition, the inhibition of RIPK1/3 activity suppressed choroidal neovascularization. Thus, Ripk3 expression and/or activity may have unique roles during normal and pathological ocular vascularization through its interactions with Caspase 8 and modulation of cell death processes.

Details

Language :
English
ISSN :
20734409
Volume :
13
Issue :
24
Database :
Directory of Open Access Journals
Journal :
Cells
Publication Type :
Academic Journal
Accession number :
edsdoj.bbbdfe1808d24ccdac938f37bbd311dc
Document Type :
article
Full Text :
https://doi.org/10.3390/cells13242109