The role of shear stress in atherosclerosis: action through gene expression and inflammation?
Atherosclerotic lesions preferentially localize near side branches or curved vessels. During the last few decades, research has been shown that low or low and oscillating shear stress is associated with plaque location. Despite ample evidence, the precise mechanism is unknown. This is mainly because of a lack of appropriate animal models. We describe two novel methods to study the hypothesis that shear stress acts through endothelial gene expression or shear stress acts through localizing of inflammation. Both literature evidence and own findings support a role for both mechanisms in atherosclerosis.
Department of Biomedical Engineering, InterUniversity Institute of Cardiology of the Netherlands, Utrecht, GE Rotterdam, The Netherlands.
Caroline
C
Cheng
Rini
R
de Crom
Rien
R
van Haperen
Frank
F
Helderman
Babak
B
Mousavi Gourabi
Luc C A
LC
van Damme
Sharon W
SW
Kirschbaum
Cornelis J
CJ
Slager
Anton F W
AF
van der Steen
Rob
R
Krams
D000818:Animals; D050197:Atherosclerosis / Q000378:metabolism / Q000473:pathology*; D001808:Blood Vessels / Q000378:metabolism; D004195:Disease Models, Animal; D015971:Gene Expression Regulation, Enzymologic; D049452:Green Fluorescent Proteins / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000473:pathology*; D051379:Mice; D008954:Models, Biological; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D009991:Oscillometry; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D013314:Stress, Mechanical; D013482:Superoxide Dismutase / Q000378:metabolism
D049452:Green Fluorescent Proteins; D052250:Nitric Oxide Synthase Type III; D011451:Prostaglandin-Endoperoxide Synthases; D013482:Superoxide Dismutase