Ontology highlight
ABSTRACT:
INSTRUMENT(S): LTQ Orbitrap
ORGANISM(S): Mus Musculus (mouse)
TISSUE(S): Aortic Smooth Muscle, Aortic Smooth Muscle Cell
DISEASE(S): Aortic Atherosclerosis
SUBMITTER: Xiaoke Yin
LAB HEAD: Manuel Mayr
PROVIDER: PXD003938 | Pride | 2016-05-06
REPOSITORIES: Pride
Action | DRS | |||
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A29_1_01.RAW | Raw | |||
A29_1_01.dat-pride.pride.mgf.gz | Mgf | |||
A29_1_01.dat-pride.pride.mztab.gz | Mztab | |||
A29_1_01.dat-pride.xml.gz | Xml | |||
A29_1_02.RAW | Raw |
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Ulrich Victoria V Rotllan Noemi N Araldi Elisa E Luciano Amelia A Skroblin Philipp P Abonnenc Mélanie M Perrotta Paola P Yin Xiaoke X Bauer Ashley A Leslie Kristen L KL Zhang Pei P Aryal Binod B Montgomery Rusty L RL Thum Thomas T Martin Kathleen K Suarez Yajaira Y Mayr Manuel M Fernandez-Hernando Carlos C Sessa William C WC
EMBO molecular medicine 20160601 6
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, an ...[more]