Vascular endothelial and smooth muscle cell galvanotactic response and differential migratory behavior.

Exp Cell Res

Department of Medicine, Sarver Heart Center, College of Medicine, University of Arizona, Tucson, AZ, 85721, USA; Department of Biomedical Engineering, University of Arizona, Tucson, AZ, 85721, USA; Department of Materials Science and Engineering, University of Arizona, Tucson, AZ, 85721, USA. Electronic address:

Published: February 2021

Chronic disease or injury of the vasculature impairs the functionality of vascular wall cells particularly in their ability to migrate and repair vascular surfaces. Under pathologic conditions, vascular endothelial cells (ECs) lose their non-thrombogenic properties and decrease their motility. Alternatively, vascular smooth muscle cells (SMCs) may increase motility and proliferation, leading to blood vessel luminal invasion. Current therapies to prevent subsequent blood vessel occlusion commonly mechanically injure vascular cells leading to endothelial denudation and smooth muscle cell luminal migration. Due to this dichotomous migratory behavior, a need exists for modulating vascular cell growth and migration in a more targeted manner. Here, we examine the efficacy of utilizing small direct current electric fields to influence vascular cell-specific migration ("galvanotaxis"). We designed, fabricated, and implemented an in vitro chamber for tracking vascular cell migration direction, distance, and displacement under galvanotactic influence of varying magnitude. Our results indicate that vascular ECs and SMCs have differing responses to galvanotaxis; ECs exhibit a positive correlation of anodal migration while SMCs exhibit minimal change in directional migration in relation to the electric field direction. SMCs exhibit less motility response (i.e. distance traveled in 4 h) compared to ECs, but SMCs show a significantly higher motility at low electric potentials (80 mV/cm). With further investigation and translation, galvanotaxis may be an effective solution for modulation of vascular cell-specific migration, leading to enhanced endothelialization, with coordinate reduced smooth muscle in-migration.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7906251PMC
http://dx.doi.org/10.1016/j.yexcr.2020.112447DOI Listing

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