Loss of Endothelial APOE4 Dysregulates Neural Function In Vivo

Background We recently found that loss of endothelial cell APOE3 disrupts neurovascular and synaptic function. However, whether endothelial APOE4 is detrimental or protective for neural function under physiological conditions is unknown. Therefore, the goal of this study was to determine the role of...

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Main Authors: Felecia M. Marottoli, Deebika Balu, Eden Flores‐Barrera, Emilce Artur de la Villarmois, Hui Zhang, Rohan Chaudhary, Ruju Talati, Kuei Y. Tseng, Leon M. Tai
Format: Article
Language:English
Published: Wiley 2024-12-01
Series:Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
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Online Access:https://www.ahajournals.org/doi/10.1161/JAHA.124.035080
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author Felecia M. Marottoli
Deebika Balu
Eden Flores‐Barrera
Emilce Artur de la Villarmois
Hui Zhang
Rohan Chaudhary
Ruju Talati
Kuei Y. Tseng
Leon M. Tai
author_facet Felecia M. Marottoli
Deebika Balu
Eden Flores‐Barrera
Emilce Artur de la Villarmois
Hui Zhang
Rohan Chaudhary
Ruju Talati
Kuei Y. Tseng
Leon M. Tai
author_sort Felecia M. Marottoli
collection DOAJ
description Background We recently found that loss of endothelial cell APOE3 disrupts neurovascular and synaptic function. However, whether endothelial APOE4 is detrimental or protective for neural function under physiological conditions is unknown. Therefore, the goal of this study was to determine the role of endothelial cell APOE4 in regulating brain function in vivo. Methods and Results We developed APOE4fl/fl/Cdh5(PAC)‐CreERT2+/− and APOE4fl/fl/Cdh5(PAC)‐CreERT2−/− (control) mice. Knockdown of endothelial cell APOE4 was induced at ≈4 to 5 weeks of age. Experiments were conducted at 9 months of age to evaluate neurovascular and neuronal function via biochemistry, immunohistochemistry, behavior tests, and electrophysiology. Endothelial cell APOE4 knockdown resulted in higher neurovascular permeability, lower claudin‐5 vessel coverage, impaired trace fear memory extinction, and disruption of cortical excitatory‐inhibitory balance of synaptic activity. Conclusions Our data support the novel concept that endothelial cell APOE4 is protective for brain function when other cell types express APOE4.
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spelling doaj-art-3e6a235431fc4a1e9f1c0e000b3adf6a2024-12-03T10:06:25ZengWileyJournal of the American Heart Association: Cardiovascular and Cerebrovascular Disease2047-99802024-12-01132310.1161/JAHA.124.035080Loss of Endothelial APOE4 Dysregulates Neural Function In VivoFelecia M. Marottoli0Deebika Balu1Eden Flores‐Barrera2Emilce Artur de la Villarmois3Hui Zhang4Rohan Chaudhary5Ruju Talati6Kuei Y. Tseng7Leon M. Tai8Department of Anatomy and Cell Biology University of Illinois at Chicago Chicago IL USADepartment of Anatomy and Cell Biology University of Illinois at Chicago Chicago IL USADepartment of Anatomy and Cell Biology University of Illinois at Chicago Chicago IL USADepartment of Anatomy and Cell Biology University of Illinois at Chicago Chicago IL USADepartment of Anatomy and Cell Biology University of Illinois at Chicago Chicago IL USADepartment of Anatomy and Cell Biology University of Illinois at Chicago Chicago IL USADepartment of Anatomy and Cell Biology University of Illinois at Chicago Chicago IL USADepartment of Anatomy and Cell Biology University of Illinois at Chicago Chicago IL USADepartment of Anatomy and Cell Biology University of Illinois at Chicago Chicago IL USABackground We recently found that loss of endothelial cell APOE3 disrupts neurovascular and synaptic function. However, whether endothelial APOE4 is detrimental or protective for neural function under physiological conditions is unknown. Therefore, the goal of this study was to determine the role of endothelial cell APOE4 in regulating brain function in vivo. Methods and Results We developed APOE4fl/fl/Cdh5(PAC)‐CreERT2+/− and APOE4fl/fl/Cdh5(PAC)‐CreERT2−/− (control) mice. Knockdown of endothelial cell APOE4 was induced at ≈4 to 5 weeks of age. Experiments were conducted at 9 months of age to evaluate neurovascular and neuronal function via biochemistry, immunohistochemistry, behavior tests, and electrophysiology. Endothelial cell APOE4 knockdown resulted in higher neurovascular permeability, lower claudin‐5 vessel coverage, impaired trace fear memory extinction, and disruption of cortical excitatory‐inhibitory balance of synaptic activity. Conclusions Our data support the novel concept that endothelial cell APOE4 is protective for brain function when other cell types express APOE4.https://www.ahajournals.org/doi/10.1161/JAHA.124.035080ApoE4behaviorbrain endothelial cells
spellingShingle Felecia M. Marottoli
Deebika Balu
Eden Flores‐Barrera
Emilce Artur de la Villarmois
Hui Zhang
Rohan Chaudhary
Ruju Talati
Kuei Y. Tseng
Leon M. Tai
Loss of Endothelial APOE4 Dysregulates Neural Function In Vivo
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
ApoE4
behavior
brain endothelial cells
title Loss of Endothelial APOE4 Dysregulates Neural Function In Vivo
title_full Loss of Endothelial APOE4 Dysregulates Neural Function In Vivo
title_fullStr Loss of Endothelial APOE4 Dysregulates Neural Function In Vivo
title_full_unstemmed Loss of Endothelial APOE4 Dysregulates Neural Function In Vivo
title_short Loss of Endothelial APOE4 Dysregulates Neural Function In Vivo
title_sort loss of endothelial apoe4 dysregulates neural function in vivo
topic ApoE4
behavior
brain endothelial cells
url https://www.ahajournals.org/doi/10.1161/JAHA.124.035080
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