Journal
NUTRIENTS
Volume 14, Issue 21, Pages -Publisher
MDPI
DOI: 10.3390/nu14214518
Keywords
resveratrol; endothelial cell; inflammation; atherosclerosis; PHACTR1
Categories
Funding
- National Key R&D Program of China [2021YFC2500500]
- National Natural Science Foundation of China [82070464, 81941022, 81530025, 81903606]
- Strategic Priority Research Program of Chinese Academy of Sciences [XDB38010100]
- Program for Innovative Research Team of The First Affiliated Hospital of USTC [CXGG02]
- Anhui Provincial Key Research and Development Program [202104j07020051]
- Anhui Province Science Fund for Distinguished Young Scholars [2208085J08]
- Local Innovative and Research Teams Project of Guangdong Pearl River Talents Program [2017BT01S131]
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Atherosclerosis is a chronic inflammatory vascular disease in which endothelial cells play a crucial role. Resveratrol, a polyphenol, prevents cardiovascular disease by regulating multiple signaling pathways. The study suggests that resveratrol may serve as a shear stress mimetic drug for combating atherosclerosis.
Atherosclerosis is a chronic inflammatory vascular disease in which endothelial cells play an important role in maintaining vascular homeostasis. Endotheliitis caused by endothelial dysfunction (ED) is the key cause for the development of cardiovascular and cerebrovascular diseases as well as other vascular system diseases. Resveratrol (RES), a multi-functional polyphenol present in edible plants and fruits, prevents cardiovascular disease by regulating a variety of athero-relevant signaling pathways. By transcriptome profiling of RES-treated human umbilical vein endothelial cells (HUVECs) and in-depth bioinformatic analysis, we observed that differentially expressed genes (DEGs) were enriched in KEGG pathways of fluid shear stress and atherosclerosis, suggesting that the RES may serve as a good template for a shear stress mimetic drug that hold promise in combating atherosclerosis. A heat map and multiple datasets superimposed screening revealed that RES significantly down-regulated phosphatase and actin modulator 1 (PHACTR1), a pivotal coronary artery disease risk gene associated with endothelial inflammation and polyvascular diseases. We further demonstrate that RES down-regulated the gene and protein expression of PHACTR1 and inhibited TNF-alpha-induced adhesion of THP-1 monocytes to activated endothelial cells via suppressing the expression of PHACTR1. Taken together, our study reveals that PHACTR1 represents a new molecular target for RES to maintain endothelial cell homeostasis and prevent atherosclerotic cardiovascular disease.
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