MiR-195 inhibits macrophages pro-inflammatory profile and impacts the crosstalk with smooth muscle cells.
Ontology highlight
ABSTRACT: Macrophages are a main component of atherosclerotic plaques. Recent studies suggest that pro-inflammatory M1 macrophages are pro-atherogenic while M2 macrophages promote plaque stability. Moreover, toll-like receptor signalling pathways are implicated in atherosclerotic plaque formation, evolution and regression. We propose microRNAs as key regulators of these processes. In this context, our goal is to promote inflammation resolution using miR-195 to reduce M1-like macrophage polarization and to evaluate the molecular mechanisms underlying such effect, as well as to explore the functional consequences for smooth muscle cell recruitment. Human primary macrophages were differentiated from peripheral blood monocytes and stimulated with LPS or IL-10 to promote M1 or M2c polarization, respectiv
SUBMITTER: Bras JP
PROVIDER: S-EPMC5699821 | biostudies-literature | 2017
REPOSITORIES: biostudies-literature
ACCESS DATA