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Mouse Smooth muscle cell secretome with Anti-miR / pre-miR treatment

ABSTRACT: Overexpression and inhibition of miR-29 (pre-miR and anti-miR to miR-29b) in murine aortic smooth muscle cells, analysis of their secretome (conditioned media after serum starvation), n=3 for all four groups (pre-miR control, pre-miR-29b, anti-miR control, anti-miR-29b).

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

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Dataset's files

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			Action	DRS
	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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Publications

Chronic miR-29 antagonism promotes favorable plaque remodeling in atherosclerotic mice.

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]

PMID: 27137489

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