Macrophages regulate vascular smooth muscle cell function during atherosclerosis progression through IL-1β/STAT3 signaling

Vascular smooth muscle cells (VSMCs) play a central role in atherosclerosis progression, but the functional changes in VSMCs and the associated cellular crosstalk during atherosclerosis progression remain unknown. Here we show that scRNA-seq analysis of proximal adjacent (PA) and atherosclerotic cor...

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Published in:Communications biology Vol. 5; no. 1; pp. 1316 - 16
Main Authors: Xue, Yuzhou, Luo, Minghao, Hu, Xiankang, Li, Xiang, Shen, Jian, Zhu, Wenyan, Huang, Longxiang, Hu, Yu, Guo, Yongzheng, Liu, Lin, Wang, Lingbang, Luo, Suxin
Format: Journal Article
Language:English
Published: London Nature Publishing Group UK 01.12.2022
Nature Publishing Group
Nature Portfolio
Subjects:
13
13/1
13/89
14
14/32
38
38/91
64
64/60
692/4019/592/2727
692/4019/592/75
82
96
96/63
Apoptosis
Arteriosclerosis
Atherosclerosis
Biology
Biomedical and Life Sciences
Carotid arteries
Carotid artery
Humans
IL-1β
Leukocyte Count
Life Sciences
Macrophages
Muscle, Smooth, Vascular
Myocytes, Smooth Muscle
Phenotypes
Plaques
Smooth muscle
Stat3 protein
STAT3 Transcription Factor
Transcription factors
ISSN:2399-3642, 2399-3642
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Abstract Vascular smooth muscle cells (VSMCs) play a central role in atherosclerosis progression, but the functional changes in VSMCs and the associated cellular crosstalk during atherosclerosis progression remain unknown. Here we show that scRNA-seq analysis of proximal adjacent (PA) and atherosclerotic core (AC) regions of human carotid artery plaques identifies functional alterations in macrophage-like VSMCs, elucidating the main state differences between PA and AC VSMCs. And, IL-1β mediates macrophage-macrophage-like VSMC crosstalk through regulating key transcription factors involved in macrophage-like VSMCs functional alterations during atherosclerosis progression. In vitro assays reveal VSMCs trans-differentiated into a macrophage-like phenotype and then functional alterations in response to macrophage-derived stimuli. IL-1β promots the adhesion, inflammation, and apoptosis of macrophage-like VSMCs in a STAT3 dependent manner. The current findings provide interesting insight into the macrophages-macrophage-like VSMC crosstalk, which would drive functional alterations in the latter cell type through IL-1β/STAT3 axis during atherosclerosis progression. Characterisation of macrophages from human carotid artery plaques and in vitro assays reveal that macrophages regulate vascular smooth muscle cell function during atherosclerosis progression through the IL-1β/STAT3 axis.
AbstractList Vascular smooth muscle cells (VSMCs) play a central role in atherosclerosis progression, but the functional changes in VSMCs and the associated cellular crosstalk during atherosclerosis progression remain unknown. Here we show that scRNA-seq analysis of proximal adjacent (PA) and atherosclerotic core (AC) regions of human carotid artery plaques identifies functional alterations in macrophage-like VSMCs, elucidating the main state differences between PA and AC VSMCs. And, IL-1β mediates macrophage-macrophage-like VSMC crosstalk through regulating key transcription factors involved in macrophage-like VSMCs functional alterations during atherosclerosis progression. In vitro assays reveal VSMCs trans-differentiated into a macrophage-like phenotype and then functional alterations in response to macrophage-derived stimuli. IL-1β promots the adhesion, inflammation, and apoptosis of macrophage-like VSMCs in a STAT3 dependent manner. The current findings provide interesting insight into the macrophages-macrophage-like VSMC crosstalk, which would drive functional alterations in the latter cell type through IL-1β/STAT3 axis during atherosclerosis progression.
Vascular smooth muscle cells (VSMCs) play a central role in atherosclerosis progression, but the functional changes in VSMCs and the associated cellular crosstalk during atherosclerosis progression remain unknown. Here we show that scRNA-seq analysis of proximal adjacent (PA) and atherosclerotic core (AC) regions of human carotid artery plaques identifies functional alterations in macrophage-like VSMCs, elucidating the main state differences between PA and AC VSMCs. And, IL-1β mediates macrophage-macrophage-like VSMC crosstalk through regulating key transcription factors involved in macrophage-like VSMCs functional alterations during atherosclerosis progression. In vitro assays reveal VSMCs trans-differentiated into a macrophage-like phenotype and then functional alterations in response to macrophage-derived stimuli. IL-1β promots the adhesion, inflammation, and apoptosis of macrophage-like VSMCs in a STAT3 dependent manner. The current findings provide interesting insight into the macrophages-macrophage-like VSMC crosstalk, which would drive functional alterations in the latter cell type through IL-1β/STAT3 axis during atherosclerosis progression.Vascular smooth muscle cells (VSMCs) play a central role in atherosclerosis progression, but the functional changes in VSMCs and the associated cellular crosstalk during atherosclerosis progression remain unknown. Here we show that scRNA-seq analysis of proximal adjacent (PA) and atherosclerotic core (AC) regions of human carotid artery plaques identifies functional alterations in macrophage-like VSMCs, elucidating the main state differences between PA and AC VSMCs. And, IL-1β mediates macrophage-macrophage-like VSMC crosstalk through regulating key transcription factors involved in macrophage-like VSMCs functional alterations during atherosclerosis progression. In vitro assays reveal VSMCs trans-differentiated into a macrophage-like phenotype and then functional alterations in response to macrophage-derived stimuli. IL-1β promots the adhesion, inflammation, and apoptosis of macrophage-like VSMCs in a STAT3 dependent manner. The current findings provide interesting insight into the macrophages-macrophage-like VSMC crosstalk, which would drive functional alterations in the latter cell type through IL-1β/STAT3 axis during atherosclerosis progression.
Vascular smooth muscle cells (VSMCs) play a central role in atherosclerosis progression, but the functional changes in VSMCs and the associated cellular crosstalk during atherosclerosis progression remain unknown. Here we show that scRNA-seq analysis of proximal adjacent (PA) and atherosclerotic core (AC) regions of human carotid artery plaques identifies functional alterations in macrophage-like VSMCs, elucidating the main state differences between PA and AC VSMCs. And, IL-1β mediates macrophage-macrophage-like VSMC crosstalk through regulating key transcription factors involved in macrophage-like VSMCs functional alterations during atherosclerosis progression. In vitro assays reveal VSMCs trans-differentiated into a macrophage-like phenotype and then functional alterations in response to macrophage-derived stimuli. IL-1β promots the adhesion, inflammation, and apoptosis of macrophage-like VSMCs in a STAT3 dependent manner. The current findings provide interesting insight into the macrophages-macrophage-like VSMC crosstalk, which would drive functional alterations in the latter cell type through IL-1β/STAT3 axis during atherosclerosis progression.Characterisation of macrophages from human carotid artery plaques and in vitro assays reveal that macrophages regulate vascular smooth muscle cell function during atherosclerosis progression through the IL-1β/STAT3 axis.
Vascular smooth muscle cells (VSMCs) play a central role in atherosclerosis progression, but the functional changes in VSMCs and the associated cellular crosstalk during atherosclerosis progression remain unknown. Here we show that scRNA-seq analysis of proximal adjacent (PA) and atherosclerotic core (AC) regions of human carotid artery plaques identifies functional alterations in macrophage-like VSMCs, elucidating the main state differences between PA and AC VSMCs. And, IL-1β mediates macrophage-macrophage-like VSMC crosstalk through regulating key transcription factors involved in macrophage-like VSMCs functional alterations during atherosclerosis progression. In vitro assays reveal VSMCs trans-differentiated into a macrophage-like phenotype and then functional alterations in response to macrophage-derived stimuli. IL-1β promots the adhesion, inflammation, and apoptosis of macrophage-like VSMCs in a STAT3 dependent manner. The current findings provide interesting insight into the macrophages-macrophage-like VSMC crosstalk, which would drive functional alterations in the latter cell type through IL-1β/STAT3 axis during atherosclerosis progression. Characterisation of macrophages from human carotid artery plaques and in vitro assays reveal that macrophages regulate vascular smooth muscle cell function during atherosclerosis progression through the IL-1β/STAT3 axis.
Characterisation of macrophages from human carotid artery plaques and in vitro assays reveal that macrophages regulate vascular smooth muscle cell function during atherosclerosis progression through the IL-1β/STAT3 axis.
ArticleNumber 1316
Author Shen, Jian
Guo, Yongzheng
Wang, Lingbang
Zhu, Wenyan
Huang, Longxiang
Luo, Minghao
Li, Xiang
Hu, Xiankang
Luo, Suxin
Xue, Yuzhou
Hu, Yu
Liu, Lin
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  fullname: Luo, Suxin
  email: luosuxin0204@163.com
  organization: Department of Cardiology, the First Affiliated Hospital of Chongqing Medical University
BackLink https://www.ncbi.nlm.nih.gov/pubmed/36456628$$D View this record in MEDLINE/PubMed
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Snippet Vascular smooth muscle cells (VSMCs) play a central role in atherosclerosis progression, but the functional changes in VSMCs and the associated cellular...
Characterisation of macrophages from human carotid artery plaques and in vitro assays reveal that macrophages regulate vascular smooth muscle cell function...
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Title Macrophages regulate vascular smooth muscle cell function during atherosclerosis progression through IL-1β/STAT3 signaling
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