Atherosclerosis Models

A Method to Culture Endothelial Cells in the Presence of Cyclic Waveforms 

Download this poster to learn how to develop physiologically relevant athero-prone and athero-protective endothelial cell models.

Poster highlights include:

  • Using shear stress to simulate the effects of atherosclerosis on different areas of the vasculature
  • The differences in the impact of continuous or pulsatile shear flow on endothelial cell organization
  • How to improve the physiological relevance of cell culture models 
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Atherosclerosis modeling with BioFlux

Plaque buildup in the arteries, caused by atherosclerosis, can lead to extreme complications in the body. These plaques – buildups of fats, cholesterol, and other molecules – can constrict blood flow and cause clotting. Fortunately, atherosclerosis can be preventable, and it is treatable. Exploring artery injury and plaque formation in atherosclerosis models will help further propel researchers to discover the root of the issue. Platelets adhering to endothelial cells or collagen function as the directors of inflammation, orchestrating the movement of immune cells and progenitor cells to the site of injury.

Analyzing these models of atherosclerosis in vitro is crucial to fully comprehend the intricacies of atherogenesis and vascular inflammation. By controlling conditions such as temperature, pressure, and flow, the BioFlux microfluidic well plate design can mimic processes that occur in the vasculature. Platelet behavior and thrombosis is easily simulated with the use of whole blood, coagulants, and other necessary compounds used to study atherosclerosis.

Anti-coagulated blood was treated with water or NSC23766, a Rac1 inhibitor, and perfused over plaque-coated BioFlux well plate channels at ambient temperature for 10 mins (shear rate 1500 s-1). (A) Fluorescent images of the control and NSC23766 channels 10 minutes after beginning of blood flow. (B) NSC23766 significantly inhibited platelet secretion (Siess et al., 2010).
Ginkgolide B, a Ginkgo biloba leaf extract inhibits platelet activation by binding the platelet-activating factor receptor (PAFR). Under different levels of shear stress (1 and 9 dyn/cm^2), Ginkgolide B reduced platelet adhesion in TNFα-treated HUVECs (Qi et al., 2018).

Key BioFlux Advantages For Atherosclerosis Studies