Quantifying effects of cyclic stretch on cell–collagen substrate adhesiveness of vascular endothelial cells. (May 2018)

• Record Type: Journal Article
• Authors: Omidvar, Ramin; Tafazzoli-Shadpour, Mohammad; Mahmoodi-Nobar, Farbod; Azadi, Shohreh; Khani, Mohammad-Mehdi
• Is Part Of: Proceedings of the Institution of Mechanical Engineers. Volume 232:Number 5(2018:May)
• Page Start: 531
• Page End: 541
• Publication Date: 2018-05
• Subjects: HUVECs -- mechanobiology -- cell adhesion -- atomic force microscopy -- single-cell force spectroscopy; Biomedical engineering -- Periodicals; Medical instruments and apparatus -- Periodicals; 610.28
• DOI: 10.1177/0954411918767477
• Languages: English
• ISSNs: 0954-4119

Abstract

Vascular endothelium is continuously subjected to mechanical stimulation in the form of shear forces due to blood flow as well as tensile forces as a consequence of blood pressure. Such stimuli influence endothelial behavior and regulate cell–tissue interaction for an optimized functionality. This study aimed to quantify influence of cyclic stretch on the adhesive property and stiffness of endothelial cells. The 10% cyclic stretch with frequency of 1 Hz was applied to a layer of endothelial cells cultured on a polydimethylsiloxane substrate. Cell–substrate adhesion of endothelial cells was examined by the novel approach of atomic force microscope–based single-cell force spectroscopy and cell stiffness was measured by atomic force microscopy. Furthermore, the adhesive molecular bonds were evaluated using modified Hertz contact theory. Our results show that overall adhesion of endothelial cells with substrate decreased after cyclic stretch while they became stiffer. Based on the experimental results and theoretical modeling, the decrease in the number of molecular bonds after cyclic stretch was quantified. In conclusion, in vitro cyclic stretch caused alterations in both adhesive capacity and elastic modulus of endothelial cells through mechanotransductive pathways as two major determinants of the function of these cells within the cardiovascular system.