Transient receptor potential vanilloid 4 channel deletion regulates pathological but not developmental retinal angiogenesis.
Title
Transient receptor potential vanilloid 4 channel deletion regulates pathological but not developmental retinal angiogenesis.
Creator
Cappelli HC;Guarino BD;Kanugula AK;Adapala R K;Perera V;Smith MA;Paruchuri S;Thodeti CK
Publisher
Journal of Cellular Physiology
Date
2020
2020-10-20
Description
Transient receptor potential vanilloid 4 (TRPV4) channels are mechanosensitive ion channels that regulate systemic endothelial cell (EC) functions such as vasodilation, permeability, and angiogenesis. TRPV4 is expressed in retinal ganglion cells, Müller glia, pigment epithelium, microvascular ECs, and modulates cell volume regulation, calcium homeostasis, and survival. TRPV4-mediated physiological or pathological retinal angiogenesis remains poorly understood. Here, we demonstrate that TRPV4 is expressed, functional, and mechanosensitive in retinal ECs. The genetic deletion of TRPV4 did not affect postnatal developmental angiogenesis but increased pathological neovascularization in response to oxygen-induced retinopathy (OIR). Retinal vessels from TRPV4 knockout mice subjected to OIR exhibited neovascular tufts that projected into the vitreous humor and displayed reduced pericyte coverage compared with wild-type mice. These results suggest that TRPV4 is a regulator of retinal angiogenesis, its deletion augments pathological retinal angiogenesis, and that TRPV4 could be a novel target for the development of therapies against neovascular ocular diseases.
Subject
neovascularization; TRPV4; mechanotransduction; ECM stiffness; human retinal endothelial cells
Identifier
Format
journalArticle
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ISSN
1097-4652 0021-9541
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October 2020 List
Citation
Cappelli HC;Guarino BD;Kanugula AK;Adapala R K;Perera V;Smith MA;Paruchuri S;Thodeti CK, “Transient receptor potential vanilloid 4 channel deletion regulates pathological but not developmental retinal angiogenesis.,” NEOMED Bibliography Database, accessed September 7, 2024, https://neomed.omeka.net/items/show/11340.