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A macrophage-specific lncRNA regulates apoptosis and atherosclerosis by tethering HuR in the nucleusSimion, Viorel; Zhou, Haoyang; Haemmig, Stefan; Pierce, Jacob B; Mendes, Shanelle; Tesmenitsky, Yevgenia; Pérez-Cremades, Daniel; Lee, James F; Chen, Alex F; Ronda, Nicoletta; Papotti, Bianca; Marto, Jarrod A; Feinberg, Mark W
Nature communications, 12/2020, Letnik: 11, Številka: 1Journal Article
Long non-coding RNAs (lncRNAs) are emerging regulators of pathophysiological processes including atherosclerosis. Using RNA-seq profiling of the intima of lesions, here we identify a macrophage-specific lncRNA MAARS (Macrophage-Associated Atherosclerosis lncRNA Sequence). Aortic intima expression of MAARS increases by 270-fold with atherosclerotic progression and decreases with regression by 60%. MAARS knockdown reduces atherosclerotic lesion formation by 52% in LDLR mice, largely independent of effects on lipid profile and inflammation, but rather by decreasing macrophage apoptosis and increasing efferocytosis in the vessel wall. MAARS interacts with HuR/ELAVL1, an RNA-binding protein and important regulator of apoptosis. Overexpression and knockdown studies verified MAARS as a critical regulator of macrophage apoptosis and efferocytosis in vitro, in an HuR-dependent manner. Mechanistically, MAARS knockdown alters HuR cytosolic shuttling, regulating HuR targets such as p53, p27, Caspase-9, and BCL2. These findings establish a mechanism by which a macrophage-specific lncRNA interacting with HuR regulates apoptosis, with implications for a broad range of vascular disease states.
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