The Role of Endothelial L-PGDS in the Pro-Angiogenic and Anti-Inflammatory Effects of Low-Dose Alcohol Consumption

Light alcohol consumption (LAC) may reduce the incidence and improve the prognosis of ischemic stroke. Recently, we found that LAC promotes cerebral angiogenesis and inhibits early inflammation following ischemic stroke. In addition, LAC upregulates lipocalin-type prostaglandin D2 synthase (L-PGDS)...

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Main Authors: Jiyu Li, Chun Li, Utsab Subedi, Pushpa Subedi, Manikandan Panchatcharam, Hong Sun
Format: Article
Language:English
Published: MDPI AG 2024-12-01
Series:Cells
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Online Access:https://www.mdpi.com/2073-4409/13/23/2007
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author Jiyu Li
Chun Li
Utsab Subedi
Pushpa Subedi
Manikandan Panchatcharam
Hong Sun
author_facet Jiyu Li
Chun Li
Utsab Subedi
Pushpa Subedi
Manikandan Panchatcharam
Hong Sun
author_sort Jiyu Li
collection DOAJ
description Light alcohol consumption (LAC) may reduce the incidence and improve the prognosis of ischemic stroke. Recently, we found that LAC promotes cerebral angiogenesis and inhibits early inflammation following ischemic stroke. In addition, LAC upregulates lipocalin-type prostaglandin D2 synthase (L-PGDS) in the brain. Thus, we determined the role of endothelial L-PGDS in the protective effect of LAC. In in vitro studies, chronic exposure to low-concentration ethanol upregulated L-PGDS and significantly increased the proliferation in cultured C57BL/6J mouse brain microvascular endothelial cells (MBMVECs). AT-56, a selective L-PGDS inhibitor, abolished low-concentration ethanol exposure-induced proliferation. In in vivo studies, 8-week gavage feeding with 0.7 g/kg/day ethanol, defined as LAC, promoted cerebral angiogenesis under physiological conditions and following ischemic stroke in male C57BL/6J mice. In addition, LAC inhibited the post-ischemic expression of adhesion molecules, neutrophil infiltration, and microglial activation. AT-56 and endothelial cell (EC)-specific L-PGDS conditional knockout did not significantly alter cerebral angiogenesis and post-ischemic inflammation in the control mice but eliminated the pro-angiogenic and anti-inflammatory effects of LAC. Furthermore, EC-specific L-PGDS conditional knockout alleviated the neuroprotective effect of LAC against cerebral ischemia/reperfusion injury. These findings suggest that endothelial L-PGDS may be crucial in the pro-angiogenic and anti-inflammatory effects of LAC against ischemic stroke.
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spelling doaj-art-b0caca7d011e422eb79da3b42e4d4bc32025-08-20T02:38:47ZengMDPI AGCells2073-44092024-12-011323200710.3390/cells13232007The Role of Endothelial L-PGDS in the Pro-Angiogenic and Anti-Inflammatory Effects of Low-Dose Alcohol ConsumptionJiyu Li0Chun Li1Utsab Subedi2Pushpa Subedi3Manikandan Panchatcharam4Hong Sun5Department of Cellular Biology and Anatomy, LSU Health Shreveport, Shreveport, LA 71103, USADepartment of Cellular Biology and Anatomy, LSU Health Shreveport, Shreveport, LA 71103, USADepartment of Cellular Biology and Anatomy, LSU Health Shreveport, Shreveport, LA 71103, USADepartment of Cellular Biology and Anatomy, LSU Health Shreveport, Shreveport, LA 71103, USADepartment of Cellular Biology and Anatomy, LSU Health Shreveport, Shreveport, LA 71103, USADepartment of Cellular Biology and Anatomy, LSU Health Shreveport, Shreveport, LA 71103, USALight alcohol consumption (LAC) may reduce the incidence and improve the prognosis of ischemic stroke. Recently, we found that LAC promotes cerebral angiogenesis and inhibits early inflammation following ischemic stroke. In addition, LAC upregulates lipocalin-type prostaglandin D2 synthase (L-PGDS) in the brain. Thus, we determined the role of endothelial L-PGDS in the protective effect of LAC. In in vitro studies, chronic exposure to low-concentration ethanol upregulated L-PGDS and significantly increased the proliferation in cultured C57BL/6J mouse brain microvascular endothelial cells (MBMVECs). AT-56, a selective L-PGDS inhibitor, abolished low-concentration ethanol exposure-induced proliferation. In in vivo studies, 8-week gavage feeding with 0.7 g/kg/day ethanol, defined as LAC, promoted cerebral angiogenesis under physiological conditions and following ischemic stroke in male C57BL/6J mice. In addition, LAC inhibited the post-ischemic expression of adhesion molecules, neutrophil infiltration, and microglial activation. AT-56 and endothelial cell (EC)-specific L-PGDS conditional knockout did not significantly alter cerebral angiogenesis and post-ischemic inflammation in the control mice but eliminated the pro-angiogenic and anti-inflammatory effects of LAC. Furthermore, EC-specific L-PGDS conditional knockout alleviated the neuroprotective effect of LAC against cerebral ischemia/reperfusion injury. These findings suggest that endothelial L-PGDS may be crucial in the pro-angiogenic and anti-inflammatory effects of LAC against ischemic stroke.https://www.mdpi.com/2073-4409/13/23/2007alcoholL-PGDSangiogenesisinflammationischemic stroke
spellingShingle Jiyu Li
Chun Li
Utsab Subedi
Pushpa Subedi
Manikandan Panchatcharam
Hong Sun
The Role of Endothelial L-PGDS in the Pro-Angiogenic and Anti-Inflammatory Effects of Low-Dose Alcohol Consumption
Cells
alcohol
L-PGDS
angiogenesis
inflammation
ischemic stroke
title The Role of Endothelial L-PGDS in the Pro-Angiogenic and Anti-Inflammatory Effects of Low-Dose Alcohol Consumption
title_full The Role of Endothelial L-PGDS in the Pro-Angiogenic and Anti-Inflammatory Effects of Low-Dose Alcohol Consumption
title_fullStr The Role of Endothelial L-PGDS in the Pro-Angiogenic and Anti-Inflammatory Effects of Low-Dose Alcohol Consumption
title_full_unstemmed The Role of Endothelial L-PGDS in the Pro-Angiogenic and Anti-Inflammatory Effects of Low-Dose Alcohol Consumption
title_short The Role of Endothelial L-PGDS in the Pro-Angiogenic and Anti-Inflammatory Effects of Low-Dose Alcohol Consumption
title_sort role of endothelial l pgds in the pro angiogenic and anti inflammatory effects of low dose alcohol consumption
topic alcohol
L-PGDS
angiogenesis
inflammation
ischemic stroke
url https://www.mdpi.com/2073-4409/13/23/2007
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