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Matrix stiffness regulates the interactions between endothelial cells and monocytes

Weicong Chen1, Baoxiang Tian1, Jiaqi Liang1

  • 1Shanghai Jiao Tong University Affiliated Sixth People's Hospital, School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.

Biomaterials
|August 24, 2019
PubMed

Insights

Matrix stiffness influences endothelial cell (EC) interactions with monocytes, impacting vascular disease development. Stiffer matrices enhance ECs

Area of Science:

  • Biomaterials Science
  • Vascular Biology
  • Cellular Mechanics

Background:

  • Endothelial cells (ECs) form a critical barrier, and monocyte recruitment to ECs initiates vascular diseases like atherosclerosis.
  • Vascular EC functions are influenced by biochemical factors, hemodynamic forces, and matrix stiffness, which changes with aging and disease.
  • The precise role of matrix stiffness in EC-monocyte interactions remains unclear.

Purpose of the Study:

  • To investigate the impact of matrix stiffness on monocyte chemotaxis and adhesion to ECs.
  • To elucidate the molecular mechanisms, including microRNA (miRNA) involvement, mediating these stiffness-dependent interactions.

Main Methods:

  • ECs were cultured on matrices of varying stiffness (8, 20, and 40 kPa).
  • Monocyte chemotaxis and adhesion assays were performed.
  • Expression levels of vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), miR-126, and miR-222 were analyzed.
  • Inhibition of miR-126 and miR-222 was used to assess their role in mediating stiffness effects.

Main Results:

  • ECs on soft (8 kPa) and stiff (40 kPa) matrices exhibited enhanced chemotactic effects on monocytes compared to 20 kPa matrices.
  • Monocyte adhesion followed a similar pattern, correlating with increased VCAM-1 and ICAM-1 expression on softer and stiffer matrices.
  • miR-126 and miR-222 expression showed an inverse correlation with VCAM-1 and ICAM-1, respectively.
  • Inhibiting miR-126 and miR-222 abolished the matrix stiffness-dependent effects on monocyte adhesion, indicating their mediating role.

Conclusions:

  • Matrix stiffness significantly regulates EC-monocyte interactions, influencing monocyte recruitment and adhesion.
  • miR-126 and miR-222 mediate the effects of matrix stiffness on VCAM-1 and ICAM-1 expression, thereby controlling monocyte adhesion.
  • These findings offer insights into vascular disease pathogenesis, aging, and provide a basis for vascular tissue engineering and therapeutic strategies.

Keywords:
AdhesionChemotacticEndothelial cellsMonocytesStiffness

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