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An intimal-lumen model in a microfluidic device: potential platform for atherosclerosis-related studies
Fahima Akther1,2, Dimple Sajin1,3, Shehzahdi S Moonshi1,3
1Queensland Micro- and Nanotechnology, Griffith University, Nathan, Queensland 4111, Australia. h.ta@griffith.edu.au.
Lab on a Chip
|December 19, 2024
Summary
Researchers developed a novel microfluidic model simulating atherosclerosis by mimicking arterial blood flow. This tool effectively studies monocyte transmigration and foam cell formation, aiding in drug discovery for this vascular disease.
Area of Science:
- Biomedical Engineering
- Cardiovascular Research
- Microfluidics
Background:
- Atherosclerosis is a major global cause of death, characterized by chronic inflammation and vascular dysfunction.
- Current *in vitro* models lack physiologically relevant hemodynamic microenvironments and exhibit interspecies differences *in vivo*.
- Studying early atherosclerosis requires models that accurately replicate the arterial shear rate and cellular interactions.
Purpose of the Study:
- To develop a robust microfluidic intimal-lumen model for studying early atherosclerosis.
- To create a physiologically relevant microenvironment under arterial shear rate for observing monocyte transmigration and foam cell formation.
- To validate the model's utility for drug testing, specifically examining aspirin's inhibitory effects.
Main Methods:
- A microfluidic device with interconnected dual channels was designed to mimic the vascular lumen and intimal layer.
- Murine endothelial cells formed the vascular lumen, while collagen-embedded murine smooth muscle cells formed the intimal layer.
- Endothelial dysfunction was induced by TNF-α stimulation, and native low-density lipoprotein (LDL) was used to promote lipid accumulation.
Main Results:
- The model successfully induced endothelial dysfunction, monocyte adhesion, and transmigration under arterial shear rates.
- Subendothelial foam cell formation was observed under flow conditions, mimicking early atherosclerosis.
- Aspirin demonstrated a significant, dose-dependent inhibitory effect on monocyte adhesion and transmigration.
Conclusions:
- The developed microfluidic intimal-lumen model provides a physiologically relevant platform for studying early atherosclerosis.
- This model accurately replicates key pathological processes like monocyte transmigration and foam cell formation under arterial shear.
- The model serves as a valuable tool for pre-clinical drug screening and testing, as demonstrated by aspirin's efficacy.
