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:
Online Access:https://doi.org/10.15252/emmm.201506031
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author 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
author_facet 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
author_sort Victoria Ulrich
collection DOAJ
description 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.
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spelling doaj-art-dfae49429d474f239ee09a30e0002d2d2025-08-20T04:02:55ZengSpringer NatureEMBO Molecular Medicine1757-46761757-46842016-05-018664365310.15252/emmm.201506031Chronic miR‐29 antagonism promotes favorable plaque remodeling in atherosclerotic miceVictoria Ulrich0Noemi Rotllan1Elisa Araldi2Amelia Luciano3Philipp Skroblin4Mélanie Abonnenc5Paola Perrotta6Xiaoke Yin7Ashley Bauer8Kristen L Leslie9Pei Zhang10Binod Aryal11Rusty L Montgomery12Thomas Thum13Kathleen Martin14Yajaira Suarez15Manuel Mayr16Carlos Fernandez‐Hernando17William C Sessa18Vascular Biology and Therapeutics Program, Yale University School of MedicineVascular Biology and Therapeutics Program, Yale University School of MedicineVascular Biology and Therapeutics Program, Yale University School of MedicineVascular Biology and Therapeutics Program, Yale University School of MedicineKing's British Heart Foundation Centre, King's College LondonKing's British Heart Foundation Centre, King's College LondonVascular Biology and Therapeutics Program, Yale University School of MedicineKing's British Heart Foundation Centre, King's College LondonVascular Biology and Therapeutics Program, Yale University School of MedicineVascular Biology and Therapeutics Program, Yale University School of MedicineVascular Biology and Therapeutics Program, Yale University School of MedicineVascular Biology and Therapeutics Program, Yale University School of MedicinemiRagen TherapeuticsInstitute of Molecular and Translational Therapeutic Strategies, Hannover Medical SchoolVascular Biology and Therapeutics Program, Yale University School of MedicineVascular Biology and Therapeutics Program, Yale University School of MedicineKing's British Heart Foundation Centre, King's College LondonVascular Biology and Therapeutics Program, Yale University School of MedicineVascular Biology and Therapeutics Program, Yale University School of MedicineAbstract 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.https://doi.org/10.15252/emmm.201506031atherosclerosisLNAmiR‐29plaquestability
spellingShingle 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
Chronic miR‐29 antagonism promotes favorable plaque remodeling in atherosclerotic mice
EMBO Molecular Medicine
atherosclerosis
LNA
miR‐29
plaque
stability
title Chronic miR‐29 antagonism promotes favorable plaque remodeling in atherosclerotic mice
title_full Chronic miR‐29 antagonism promotes favorable plaque remodeling in atherosclerotic mice
title_fullStr Chronic miR‐29 antagonism promotes favorable plaque remodeling in atherosclerotic mice
title_full_unstemmed Chronic miR‐29 antagonism promotes favorable plaque remodeling in atherosclerotic mice
title_short Chronic miR‐29 antagonism promotes favorable plaque remodeling in atherosclerotic mice
title_sort chronic mir 29 antagonism promotes favorable plaque remodeling in atherosclerotic mice
topic atherosclerosis
LNA
miR‐29
plaque
stability
url https://doi.org/10.15252/emmm.201506031
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