1. Low shear stress induces M1 macrophage polarization in murine thin-cap atherosclerotic plaques.
- Author
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Seneviratne AN, Cole JE, Goddard ME, Park I, Mohri Z, Sansom S, Udalova I, Krams R, and Monaco C
- Subjects
- Animals, Apolipoproteins E deficiency, Apolipoproteins E metabolism, Biomarkers metabolism, Carotid Arteries pathology, Female, Mice, Inbred C57BL, Cell Polarity, Macrophages pathology, Plaque, Atherosclerotic pathology, Shear Strength
- Abstract
Macrophages, a significant component of atherosclerotic plaques vulnerable to acute complications, can be pro-inflammatory (designated M1), regulatory (M2), lipid- (Mox) or Heme-induced (Mhem). We showed previously that low (LSS) and oscillatory (OSS) shear stress cause thin-cap fibroatheroma and stable smooth muscle cell-rich plaque formation respectively in ApoE-knockout (ApoE(-/-)) mice. Here we investigated whether different shear stress conditions relate to specific changes in macrophage polarization and plaque morphology by applying a shear stress-altering cast to the carotid arteries of high fat-fed ApoE(-/-) mice. The M1 markers iNOS and IRF5 were highly expressed in macrophage-rich areas of LSS lesions compared to OSS lesions 6weeks after cast placement, while the M2 marker Arginase-1, and Mox/Mhem markers HO-1 and CD163 were elevated in OSS lesions. Our data indicates shear stress could be an important determinant of macrophage polarization in atherosclerosis, with low shear promoting M1 programming., (Copyright © 2015 Elsevier Ltd. All rights reserved.)
- Published
- 2015
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