Laminar shear stress modulates endothelial luminal surface stiffness in a tissue-specific manner. Academic Article uri icon

Overview

abstract

  • OBJECTIVE: Endothelial cells form vascular beds in all organs and are exposed to a range of mechanical forces that regulate cellular phenotype. We sought to determine the role of endothelial luminal surface stiffness in tissue-specific mechanotransduction of laminar shear stress in microvascular mouse cells and the role of arachidonic acid in mediating this response. METHODS: Microvascular mouse endothelial cells were subjected to laminar shear stress at 4 dynes/cm2 for 12 hours in parallel plate flow chambers that enabled real-time optical microscopy and atomic force microscopy measurements of cell stiffness. RESULTS: Lung endothelial cells aligned parallel to flow, while cardiac endothelial cells did not. This rapid alignment was accompanied by increased cell stiffness. The addition of arachidonic acid to cardiac endothelial cells increased alignment and stiffness in response to shear stress. Inhibition of arachidonic acid in lung endothelial cells and embryonic stem cell-derived endothelial cells prevented cellular alignment and decreased cell stiffness. CONCLUSIONS: Our findings suggest that increased endothelial luminal surface stiffness in microvascular cells may facilitate mechanotransduction and alignment in response to laminar shear stress. Furthermore, the arachidonic acid pathway may mediate this tissue-specific process. An improved understanding of this response will aid in the treatment of organ-specific vascular disease.

publication date

  • May 30, 2018

Research

keywords

  • Endothelial Cells
  • Mechanotransduction, Cellular
  • Stress, Mechanical

Identity

PubMed Central ID

  • PMC6407863

Scopus Document Identifier

  • 85047825560

Digital Object Identifier (DOI)

  • 10.1111/micc.12455

PubMed ID

  • 29665185

Additional Document Info

volume

  • 25

issue

  • 5