Low shear stress induces M1 macrophage polarization in murine thin-cap atherosclerotic plaques

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 fibroathero...

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Bibliographic Details
Published in:Journal of molecular and cellular cardiology 2015-12, Vol.89 (Pt B), p.168-172
Main Authors: Seneviratne, Anusha N, Cole, Jennifer E, Goddard, Michael E, Park, Inhye, Mohri, Zahra, Sansom, Stephen, Udalova, Irina, Krams, Rob, Monaco, Claudia
Format: Article
Language:English
Subjects:
Animals
Apolipoproteins E - deficiency
Apolipoproteins E - metabolism
Atherosclerosis
Biomarkers - metabolism
Cardiovascular
Carotid Arteries - pathology
Cell Polarity
Female
Macrophage
Macrophages - pathology
Mice, Inbred C57BL
Plaque, Atherosclerotic - pathology
Shear Strength
Shear stress
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Summary: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 6 weeks 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.
ISSN:0022-2828
1095-8584
DOI:10.1016/j.yjmcc.2015.10.034