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Single‐cell transcriptional profiling of human carotid plaques reveals a subpopulation of endothelial cells associated with stroke incidences

The differences in plaque histology between symptomatic and asymptomatic patients have been widely accepted. Whether there is a heterogeneity of cells between symptomatic and asymptomatic plaques remains largely unclear. To reveal the potential heterogeneity within different plaques, which may contr...

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Autores principales: Li, Fengchan, Du, Yun, Hong, Lei, Liu, Ziting, Yan, Kunmin, Liu, Chu, Zhu, Zhen, Lu, Qiongyu, Tang, Chaojun, Zhu, Li
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9189335/
https://www.ncbi.nlm.nih.gov/pubmed/35527426
http://dx.doi.org/10.1111/jcmm.17354
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author Li, Fengchan
Du, Yun
Hong, Lei
Liu, Ziting
Yan, Kunmin
Liu, Chu
Zhu, Zhen
Lu, Qiongyu
Tang, Chaojun
Zhu, Li
author_facet Li, Fengchan
Du, Yun
Hong, Lei
Liu, Ziting
Yan, Kunmin
Liu, Chu
Zhu, Zhen
Lu, Qiongyu
Tang, Chaojun
Zhu, Li
author_sort Li, Fengchan
collection PubMed
description The differences in plaque histology between symptomatic and asymptomatic patients have been widely accepted. Whether there is a heterogeneity of cells between symptomatic and asymptomatic plaques remains largely unclear. To reveal the potential heterogeneity within different plaques, which may contribute to different stroke incidences, we obtained the scRNA‐seq data from symptomatic and asymptomatic patients and identified eight cell types present in plaques. Further analysis of endothelial cells (ECs) revealed three distinct EC subpopulations appeared to be endowed with specific biological functions such as antigen processing and presentation, cell adhesion, and smooth muscle cell proliferation. Of note, the differentially expressed genes of the EC 2 subpopulation showed that the genes involved in cell adhesion were up‐regulated in asymptomatic plaques compared to symptomatic plaques. Integrating the data of intraplaque haemorrhage and plaque stability, the 5th top‐enriched biological process was cell adhesion in the stable or non‐haemorrhaged plaques compared to unstable plaques or haemorrhaged plaques. Among these cell adhesion‐related genes, the intersection gene AOC3 may play a vital role in plaque haemorrhage and plaque stability. Targeting cell adhesion and the specialized genes may provide potential new therapeutic directions to prevent asymptomatic patients from stroke.
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spelling pubmed-91893352022-06-16 Single‐cell transcriptional profiling of human carotid plaques reveals a subpopulation of endothelial cells associated with stroke incidences Li, Fengchan Du, Yun Hong, Lei Liu, Ziting Yan, Kunmin Liu, Chu Zhu, Zhen Lu, Qiongyu Tang, Chaojun Zhu, Li J Cell Mol Med Original Articles The differences in plaque histology between symptomatic and asymptomatic patients have been widely accepted. Whether there is a heterogeneity of cells between symptomatic and asymptomatic plaques remains largely unclear. To reveal the potential heterogeneity within different plaques, which may contribute to different stroke incidences, we obtained the scRNA‐seq data from symptomatic and asymptomatic patients and identified eight cell types present in plaques. Further analysis of endothelial cells (ECs) revealed three distinct EC subpopulations appeared to be endowed with specific biological functions such as antigen processing and presentation, cell adhesion, and smooth muscle cell proliferation. Of note, the differentially expressed genes of the EC 2 subpopulation showed that the genes involved in cell adhesion were up‐regulated in asymptomatic plaques compared to symptomatic plaques. Integrating the data of intraplaque haemorrhage and plaque stability, the 5th top‐enriched biological process was cell adhesion in the stable or non‐haemorrhaged plaques compared to unstable plaques or haemorrhaged plaques. Among these cell adhesion‐related genes, the intersection gene AOC3 may play a vital role in plaque haemorrhage and plaque stability. Targeting cell adhesion and the specialized genes may provide potential new therapeutic directions to prevent asymptomatic patients from stroke. John Wiley and Sons Inc. 2022-05-08 2022-06 /pmc/articles/PMC9189335/ /pubmed/35527426 http://dx.doi.org/10.1111/jcmm.17354 Text en © 2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Li, Fengchan
Du, Yun
Hong, Lei
Liu, Ziting
Yan, Kunmin
Liu, Chu
Zhu, Zhen
Lu, Qiongyu
Tang, Chaojun
Zhu, Li
Single‐cell transcriptional profiling of human carotid plaques reveals a subpopulation of endothelial cells associated with stroke incidences
title Single‐cell transcriptional profiling of human carotid plaques reveals a subpopulation of endothelial cells associated with stroke incidences
title_full Single‐cell transcriptional profiling of human carotid plaques reveals a subpopulation of endothelial cells associated with stroke incidences
title_fullStr Single‐cell transcriptional profiling of human carotid plaques reveals a subpopulation of endothelial cells associated with stroke incidences
title_full_unstemmed Single‐cell transcriptional profiling of human carotid plaques reveals a subpopulation of endothelial cells associated with stroke incidences
title_short Single‐cell transcriptional profiling of human carotid plaques reveals a subpopulation of endothelial cells associated with stroke incidences
title_sort single‐cell transcriptional profiling of human carotid plaques reveals a subpopulation of endothelial cells associated with stroke incidences
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9189335/
https://www.ncbi.nlm.nih.gov/pubmed/35527426
http://dx.doi.org/10.1111/jcmm.17354
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