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Updated: Jul 24, 2026
Isolation of Endothelial Cells from the Lumen of Mouse Carotid Arteries for Single-Cell Multi-Omics Experiments
Published on: October 4, 2021
Integrative Single-Cell Analysis Dissects the Transcriptomic Remodeling and Altered Interaction Networks of
Mingzhen Cao1,2, Da Ke1,2, Dan Huang1,2
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, PR China.
Insights
This study reveals how endothelial cell diversity changes after myocardial infarction (MI). Targeting the Mif-Cd44 interaction in tip-like cells could improve heart function post-MI.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Single-cell Genomics
Background:
- Myocardial infarction (MI) causes significant mortality, with vascular contributions poorly understood.
- Endothelial cell diversity and function in cardiac injury require further characterization.
Purpose of the Study:
- To characterize endothelial cell reprogramming following MI using single-cell transcriptomics.
- To identify key endothelial cell-immune cell interactions and their role in cardiac dysfunction.
Main Methods:
- Integrated multi-timepoint mouse cardiac single-cell RNA sequencing data.
- Utilized scVelo, CellRank, and Dynamo for endothelial cell differentiation trajectory analysis.
- Performed in silico simulations and in vivo pharmacological inhibition experiments.
Main Results:
- Detailed transcriptome reprogramming of endothelial cell subsets post-MI.
- Identified a critical Mif-Cd44 interaction between tip-like cells and monocytes in acute MI.
- In silico Sox17 depletion simulation altered tip-like to capillary endothelial cell transition.
- In vivo Mif inhibition worsened cardiac dysfunction in a mouse MI model.
Conclusions:
- Endothelial cell heterogeneity plays a crucial role in the response to myocardial infarction.
- The Mif-Cd44 pathway represents a potential therapeutic target for mitigating cardiac dysfunction after MI.
Abstract:
Myocardial infarction (MI) is a cardiovascular disease characterized by the irreversible necrosis of myocardial cells and high morbidity and mortality rates. The vascular contributions and diversity of endothelial cells in this fatal disease are poorly characterized. Here, we integrated multiple mouse cardiac single-cell transcriptomic data from six time points after MI and characterized the transcriptome reprogramming of endothelial cell subsets. Endothelial cell subsets differentiation trajectory analysis was conducted using scVelo, CellRank, and Dynamo. In silico simulation of Sox17 depletion perturbed the phenotypic transition from tip-like cells to capillary endothelial cells. Endothelial cell and immune cell interaction analyses identified a Mif-Cd44 interaction between tip-like cells and monocytes in the acute phase. In vivo pharmacological inhibition of Mif exacerbated cardiac dysfunction in the mouse MI model.
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