Publication date: 25th July 2016
Atherosclerosis is a chronic inflammation of the arterial wall triggered by low density lipoprotein (LDL) retention due to prolonged exposure to a lipid-rich diet, which eventually leads to macrophage recruitment and activation, causing further lipid retention. Being the underlying mechanism of stroke and ischemic heart disease, atherosclerosis accounts for up to 25 % of deaths worldwide. Atherosclerosis shares several similarities with the natural process of arterial stiffening such as smooth muscle cell infiltration from the tunica media into the tunica intima, the excess deposition of collagen and crosslinking of extracellular matrix components. Although the association between arterial stiffening and atherosclerosis has been reported in several clinical studies, the direct impact of mechanical properties on lipid uptake behavior in macrophages remains unclear. In this study, we encapsulate THP-1 derived macrophages within hydrogel scaffolds of varying stiffness and expose them to lipoprotein-rich medium in vitro. This provides a biomimetic approach to elucidate how changes in mechanical stiffness during atherosclerosis affect retention of lipids in macrophages. Our results show increased cellular lipid droplet formation and overall lipid uptake with increasing matrix stiffness, which suggests a link between arterial wall stiffening and lipid retention. Further studies are aimed at identifying the mechanism of stiffness sensing and identifying if changes in scaffold stiffness result in distinct lipid biochemistry.
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