Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/154049
Title: Loss of caveolin-1 impairs light flicker-induced neurovascular coupling at the optic nerve head
Authors: Loo, Jing Hong
Lee, Ying Shi
Woon, Chang Yi
Yong, Victor H. K.
Tan, Bingyao
Schmetterer, Leopold
Chong, Rachel S.
Keywords: Engineering::Chemical engineering
Issue Date: 2021
Source: Loo, J. H., Lee, Y. S., Woon, C. Y., Yong, V. H. K., Tan, B., Schmetterer, L. & Chong, R. S. (2021). Loss of caveolin-1 impairs light flicker-induced neurovascular coupling at the optic nerve head. Frontiers in Neuroscience, 15, 764898-. https://dx.doi.org/10.3389/fnins.2021.764898
Project: Duke-NUS-KMRA/2017/0011
CNIG19nov-0011
Journal: Frontiers in Neuroscience
Abstract: Glaucoma is a neurodegenerative disease, which results in characteristic visual field defects. Intraocular pressure (IOP) remains the main risk factor for this leading cause of blindness. Recent studies suggest that disturbances in neurovascular coupling (NVC) may be associated with glaucoma. The resultant imbalance between vascular perfusion and neuronal stimulation in the eye may precede retinal ganglion cell (RGC) loss and increase the susceptibility of the eye to raised IOP and glaucomatous degeneration. Caveolin-1 (Cav-1) is an integral scaffolding membrane protein found abundantly in retinal glial and vascular tissues, with possible involvement in regulating the neurovascular coupling response. Mutations in Cav-1 have been identified as a major genetic risk factor for glaucoma. Therefore, we aim to evaluate the effects of Cav-1 depletion on neurovascular coupling, retinal vessel characteristics, RGC density and the positive scotopic threshold response (pSTR) in Cav-1 knockout (KO) versus wild type C57/Bl6 mice (WT). Following light flicker stimulation of the retina, Cav-1 KO mice showed a smaller increase in perfusion at the optic nerve head and peripapillary arteries, suggesting defective neurovascular coupling. Evaluation of the superficial capillary plexus in Cav-1 KO mice also revealed significant differences in vascular morphology with higher vessel density, junction density and decreased average vessel length. Cav-1 KO mice exhibited higher IOP and lower pSTR amplitude. However, there was no significant difference in RGC density between Cav-1 KO and wild type mice. These findings highlight the role of Cav-1 in regulating neurovascular coupling and IOP and suggest that the loss of Cav-1 may predispose to vascular dysfunction and decreased RGC signaling in the absence of structural loss. Current treatment for glaucoma relies heavily on IOP-lowering drugs, however, there is an immense potential for new therapeutic strategies that increase Cav-1 expression or augment its downstream signaling in order to avert vascular dysfunction and glaucomatous change.
URI: https://hdl.handle.net/10356/154049
ISSN: 1662-4548
DOI: 10.3389/fnins.2021.764898
Rights: © 2021 Loo, Lee, Woon, Yong, Tan, Schmetterer and Chong. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:SCBE Journal Articles

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