Therapeutic activation of endothelial sphingosine‐1‐phosphate receptor 1 by chaperone‐bound S1P suppresses proliferative retinal neovascularization

Abstract Sphingosine‐1‐phosphate (S1P), the circulating HDL‐bound lipid mediator that acts via S1P receptors (S1PR), is required for normal vascular development. The role of this signaling axis in vascular retinopathies is unclear. Here, we show in a mouse model of oxygen‐induced retinopathy (OIR) t...

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Main Authors: Colin Niaudet, Bongnam Jung, Andrew Kuo, Steven Swendeman, Edward Bull, Takahiro Seno, Reed Crocker, Zhongjie Fu, Lois E H Smith, Timothy Hla
Format: Article
Language:English
Published: Springer Nature 2023-03-01
Series:EMBO Molecular Medicine
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Online Access:https://doi.org/10.15252/emmm.202216645
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author Colin Niaudet
Bongnam Jung
Andrew Kuo
Steven Swendeman
Edward Bull
Takahiro Seno
Reed Crocker
Zhongjie Fu
Lois E H Smith
Timothy Hla
author_facet Colin Niaudet
Bongnam Jung
Andrew Kuo
Steven Swendeman
Edward Bull
Takahiro Seno
Reed Crocker
Zhongjie Fu
Lois E H Smith
Timothy Hla
author_sort Colin Niaudet
collection DOAJ
description Abstract Sphingosine‐1‐phosphate (S1P), the circulating HDL‐bound lipid mediator that acts via S1P receptors (S1PR), is required for normal vascular development. The role of this signaling axis in vascular retinopathies is unclear. Here, we show in a mouse model of oxygen‐induced retinopathy (OIR) that endothelial overexpression of S1pr1 suppresses while endothelial knockout of S1pr1 worsens neovascular tuft formation. Furthermore, neovascular tufts are increased in Apom−/− mice which lack HDL‐bound S1P while they are suppressed in ApomTG mice which have more circulating HDL‐S1P. These results suggest that circulating HDL‐S1P activation of endothelial S1PR1 suppresses neovascular pathology in OIR. Additionally, systemic administration of ApoM‐Fc‐bound S1P or a small‐molecule Gi‐biased S1PR1 agonist suppressed neovascular tuft formation. Circulating HDL‐S1P activation of endothelial S1PR1 may be a key protective mechanism to guard against neovascular retinopathies that occur not only in premature infants but also in diabetic patients and aging people.
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spelling doaj-art-baf615af7db14d7584f85d219c23d9262025-08-20T04:03:01ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842023-03-011551910.15252/emmm.202216645Therapeutic activation of endothelial sphingosine‐1‐phosphate receptor 1 by chaperone‐bound S1P suppresses proliferative retinal neovascularizationColin Niaudet0Bongnam Jung1Andrew Kuo2Steven Swendeman3Edward Bull4Takahiro Seno5Reed Crocker6Zhongjie Fu7Lois E H Smith8Timothy Hla9Department of Surgery, Vascular Biology Program, Boston Children's Hospital, Harvard Medical SchoolDepartment of Surgery, Vascular Biology Program, Boston Children's Hospital, Harvard Medical SchoolDepartment of Surgery, Vascular Biology Program, Boston Children's Hospital, Harvard Medical SchoolDepartment of Surgery, Vascular Biology Program, Boston Children's Hospital, Harvard Medical SchoolDepartment of Ophthalmology, Boston Children's Hospital, Harvard Medical SchoolDepartment of Surgery, Vascular Biology Program, Boston Children's Hospital, Harvard Medical SchoolDepartment of Surgery, Vascular Biology Program, Boston Children's Hospital, Harvard Medical SchoolDepartment of Ophthalmology, Boston Children's Hospital, Harvard Medical SchoolDepartment of Ophthalmology, Boston Children's Hospital, Harvard Medical SchoolDepartment of Surgery, Vascular Biology Program, Boston Children's Hospital, Harvard Medical SchoolAbstract Sphingosine‐1‐phosphate (S1P), the circulating HDL‐bound lipid mediator that acts via S1P receptors (S1PR), is required for normal vascular development. The role of this signaling axis in vascular retinopathies is unclear. Here, we show in a mouse model of oxygen‐induced retinopathy (OIR) that endothelial overexpression of S1pr1 suppresses while endothelial knockout of S1pr1 worsens neovascular tuft formation. Furthermore, neovascular tufts are increased in Apom−/− mice which lack HDL‐bound S1P while they are suppressed in ApomTG mice which have more circulating HDL‐S1P. These results suggest that circulating HDL‐S1P activation of endothelial S1PR1 suppresses neovascular pathology in OIR. Additionally, systemic administration of ApoM‐Fc‐bound S1P or a small‐molecule Gi‐biased S1PR1 agonist suppressed neovascular tuft formation. Circulating HDL‐S1P activation of endothelial S1PR1 may be a key protective mechanism to guard against neovascular retinopathies that occur not only in premature infants but also in diabetic patients and aging people.https://doi.org/10.15252/emmm.202216645neovascularizationSphingosine‐1‐phosphate (S1P)vascular retinopathy
spellingShingle Colin Niaudet
Bongnam Jung
Andrew Kuo
Steven Swendeman
Edward Bull
Takahiro Seno
Reed Crocker
Zhongjie Fu
Lois E H Smith
Timothy Hla
Therapeutic activation of endothelial sphingosine‐1‐phosphate receptor 1 by chaperone‐bound S1P suppresses proliferative retinal neovascularization
EMBO Molecular Medicine
neovascularization
Sphingosine‐1‐phosphate (S1P)
vascular retinopathy
title Therapeutic activation of endothelial sphingosine‐1‐phosphate receptor 1 by chaperone‐bound S1P suppresses proliferative retinal neovascularization
title_full Therapeutic activation of endothelial sphingosine‐1‐phosphate receptor 1 by chaperone‐bound S1P suppresses proliferative retinal neovascularization
title_fullStr Therapeutic activation of endothelial sphingosine‐1‐phosphate receptor 1 by chaperone‐bound S1P suppresses proliferative retinal neovascularization
title_full_unstemmed Therapeutic activation of endothelial sphingosine‐1‐phosphate receptor 1 by chaperone‐bound S1P suppresses proliferative retinal neovascularization
title_short Therapeutic activation of endothelial sphingosine‐1‐phosphate receptor 1 by chaperone‐bound S1P suppresses proliferative retinal neovascularization
title_sort therapeutic activation of endothelial sphingosine 1 phosphate receptor 1 by chaperone bound s1p suppresses proliferative retinal neovascularization
topic neovascularization
Sphingosine‐1‐phosphate (S1P)
vascular retinopathy
url https://doi.org/10.15252/emmm.202216645
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