Chronic miR‐29 antagonism promotes favorable plaque remodeling in atherosclerotic mice

Chronic miR‐29 antagonism promotes favorable plaque remodeling in atherosclerotic mice

Abstract Abnormal remodeling of atherosclerotic plaques can lead to rupture, acute myocardial infarction, and death. Enhancement of plaque extracellular matrix (ECM) may improve plaque morphology and stabilize lesions. Here, we demonstrate that chronic administration of LNA‐miR‐29 into an atheroscle...

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Main Authors: Victoria Ulrich, Noemi Rotllan, Elisa Araldi, Amelia Luciano, Philipp Skroblin, Mélanie Abonnenc, Paola Perrotta, Xiaoke Yin, Ashley Bauer, Kristen L Leslie, Pei Zhang, Binod Aryal, Rusty L Montgomery, Thomas Thum, Kathleen Martin, Yajaira Suarez, Manuel Mayr, Carlos Fernandez‐Hernando, William C Sessa
Format: Article
Language:English
Published: Springer Nature 2016-05-01
Series:EMBO Molecular Medicine
Subjects:
atherosclerosis
LNA
miR‐29
plaque
stability
Online Access:https://doi.org/10.15252/emmm.201506031
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Summary:Abstract Abnormal remodeling of atherosclerotic plaques can lead to rupture, acute myocardial infarction, and death. Enhancement of plaque extracellular matrix (ECM) may improve plaque morphology and stabilize lesions. Here, we demonstrate that chronic administration of LNA‐miR‐29 into an atherosclerotic mouse model improves indices of plaque morphology. This occurs due to upregulation of miR‐29 target genes of the ECM (col1A and col3A) resulting in reduced lesion size, enhanced fibrous cap thickness, and reduced necrotic zones. Sustained LNA‐miR‐29 treatment did not affect circulating lipids, blood chemistry, or ECM of solid organs including liver, lung, kidney, spleen, or heart. Collectively, these data support the idea that antagonizing miR‐29 may promote beneficial plaque remodeling as an independent approach to stabilize vulnerable atherosclerotic lesions.
ISSN:1757-4676
1757-4684

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