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Related Experiment Video

Updated: Sep 28, 2025

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The substrate stiffness at physiological range significantly modulates vascular cell behavior.

Sheng-Wen Zhou1, Jing Wang1, Sheng-Yu Chen2

  • 1MOE Key Laboratory of Macromolecular Synthesis and Functionalization, Department of Polymer Science and Engineering, Zhejiang University, Hangzhou 310027, China.

Colloids and Surfaces. B, Biointerfaces
|April 2, 2022
PubMed
Summary
This summary is machine-generated.

Cellular microenvironment stiffness significantly impacts vascular cells. Physiological stiffness ranges enhance vascular endothelial cells (VECs) and vascular smooth muscle cells (VSMCs) adhesion and proliferation, influencing gene expression.

Keywords:
Endothelial cellsSmooth muscle cellsSubstrate stiffness

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Area of Science:

  • Biomaterials Science
  • Cell Biology
  • Vascular Biology

Background:

  • Cellular microenvironment stiffness is implicated in vascular pathologies.
  • Existing in-vitro models often use stiffness outside the physiological range (10-100 kPa) of natural vascular tissue.
  • Substrate stiffness affects vascular endothelial cells (VECs) and vascular smooth muscle cells (VSMCs).

Purpose of the Study:

  • To investigate the effects of physiological substrate stiffness (18-86 kPa) on VECs and VSMCs.
  • To determine how stiffness within the physiological range influences vascular cell behavior and gene expression.
  • To compare the impact of stiffness changes within the physiological range versus supra-physiological ranges.

Main Methods:

  • Construction of hydrogel substrates with tunable stiffness ranging from 18 kPa to 86 kPa.
  • Culture of VECs and VSMCs on hydrogel substrates of varying physiological stiffness.
  • Assessment of cell adhesion, proliferation, nitric oxide (NO) production, cell phenotype, and gene expression.

Main Results:

  • Increased stiffness within the 18-86 kPa range significantly enhanced VEC and VSMC adhesion and proliferation.
  • Softer substrates (within the physiological range) promoted higher nitric oxide (NO) production in VECs and a healthy contraction phenotype in VSMCs.
  • A small increase in stiffness within the physiological range (18-86 kPa) induced more significant changes in gene expression (560 in VECs, 243 in VSMCs) compared to a larger increase into the supra-physiological range (86-333 kPa).

Conclusions:

  • Substrate stiffness within the physiological range (18-86 kPa) profoundly influences vascular cell behavior, adhesion, and proliferation.
  • The impact of stiffness changes is more pronounced within the physiological range than at higher stiffness values.
  • These findings highlight the importance of using physiologically relevant stiffness in in-vitro models for studying vascular cells and diseases.