Lipid crystals mechanically stimulate adjacent extracellular matrix in advanced XXXX plaques.

@entity6970 @entity20616 @entity19 @entity1417 @entity397 @entity731 @entity65
OBJECTIVE: Although lipid crystals (LCs) have received attention as a causative factor of @entity397 , the mechanisms by which they increase plaque vulnerability are unknown. We examined whether solid-state LCs physically affect the adjacent extracellular matrix (ECM) using a combination of multimodal nonlinear optical (MNLO) imaging and @entity1417 ( @entity1417 ). METHODS: The changes of ECMs affected by lipids in @entity731 arteries in @entity6970 -deficient @entity19 (n  =  32) fed a high-fat diet for 20-30 weeks were micro-anatomically visualized by a 3D MNLO imaging platform including CARS for lipids, TPEF for @entity20616 , and SHG for collagen. RESULTS AND CONCLUSION: The TPEF signal of @entity20616 was increased at the peripheral regions of LCs (<10   m) compared with foam cell regions. In order to confirm the increase of @entity20616 , biochemical assay (western blot) was performed. The protein level of @entity20616 was increased approximately 2.25-fold (p  =  0.024) in LC-rich arteries. Under the hypothesis that the increase of @entity20616 resulted from the mechanical stimulus from solid-state LCs, MNLO images were subjected to @entity1417 to simulate the displacement according to the expanding magnitude of the vessel during cardiac cycles. We found that microscale focal stress was increased specifically around the LCs. These @entity1417 results corresponded with the increase of @entity20616 observed by TPEF. These data suggest that LCs mechanically stimulate the adjacent ECM to alter the composition of ECM and cause vessel remodeling. The combination of MNLO imaging and @entity1417 has great potential to verify the mechanical predictions in @entity65 .
