Open AccessChronic miR‐29 antagonism promotes favorable plaque remodeling in atherosclerotic mice
Author(s) -
Ulrich Victoria,
Rotllan Noemi,
Araldi Elisa,
Luciano Amelia,
Skroblin Philipp,
Abonnenc Mélanie,
Perrotta Paola,
Yin Xiaoke,
Bauer Ashley,
Leslie Kristen L,
Zhang Pei,
Aryal Binod,
Montgomery Rusty L,
Thum Thomas,
Martin Kathleen,
Suarez Yajaira,
Mayr Manuel,
FernandezHernando Carlos,
Sessa William C
Publication year - 2016
Publication title -
embo molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.923
H-Index - 107
eISSN - 1757-4684
pISSN - 1757-4676
DOI - 10.15252/emmm.201506031
Subject(s) - antagonism , tissue remodeling , medicine , inflammation , receptor
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 (c ol1A 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.