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Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro
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Single cell transcriptomic analysis identifies novel vascular smooth muscle subsets under high hydrostatic pressure.

Zhenzhen Chen1, Haizeng Zhang1, Yingnan Bai2

  • 1Hypertension Center, Department of Cardiac Surgery, Fuwai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Diseases, Beijing, 100191, China.

Science China. Life Sciences
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High hydrostatic pressure transforms human aortic smooth muscle cells (HASMCs) into two novel subsets. These subsets promote inflammation and inhibit endothelial function, contributing to cardiovascular disease pathogenesis.

Keywords:
VSMCshydrostatic pressurehypertensionsingle cell RNA-seq

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Area of Science:

  • Biomedical Engineering
  • Cardiovascular Research
  • Cell Biology

Background:

  • Hypertension progression involves co-risk factors and hemodynamic changes, but direct biomechanical effects remain unclear.
  • Understanding cellular responses to sustained high pressure is crucial for elucidating cardiovascular disease mechanisms.

Purpose of the Study:

  • To investigate the biomechanical effects of high hydrostatic pressure on human aortic smooth muscle cells (HASMCs).
  • To identify novel molecular classifications and functional subsets of HASMCs under hypertensive conditions.

Main Methods:

  • Construction of a high-hydrostatic-pressure cell-culture system simulating hypertension (200 mmHg).
  • Single-cell transcriptome analysis to identify distinct HASMC clusters and gene expression profiles.
  • Analysis of chemokine and protein secretion, monocyte migration, and angiogenesis inhibition.

Main Results:

  • High hydrostatic pressure induced six distinct vascular SMC (VSMC) clusters.
  • Two novel HASMC subsets were identified: an inflammatory subset (CXCL2, CXCL3, CCL2 markers) and an endothelial-function inhibitory subset (AKR1C2, AKR1C3, SERPINF1 markers).
  • These subsets were found to be upregulated in hypertensive patients and animal models, promoting monocyte migration and inhibiting angiogenesis.

Conclusions:

  • Sustained high hydrostatic pressure directly drives VSMCs into distinct subsets.
  • These novel VSMC subsets contribute to endothelial dysfunction and cardiovascular disease pathogenesis.
  • The findings offer new molecular targets for understanding and treating hypertension-related cardiovascular diseases.