26 / 40
Page 74
Notes:
conferenceseries
.com
Volume 9
Journal of Clinical & Experimental Cardiology
ISSN: 2155-9880
October 22-24, 2018 | Rome, Italy
27
th
European Cardiology Conference
Euro Cardiology 2018
October 22-24, 2018
Deletion of miR-147 in macrophages promotes atherosclerosis
Maliheh Nazari Jahantigh
Institute for Cardiovascular Prevention - LMU, Germany
A
therosclerosis is the main cause of cardiovascular disease that are number one killer worldwide. Macrophage dysfunction
contributes to the progression of atherosclerosis and microRNAs, negative regulators of gene expression, mediate
macrophage function upon activation. miR-147 is upregulated in inflammatory macrophages as well as murine and human
atherosclerotic plaques, while it is downregulated in peripheral monocytes from patients with coronary artery disease.
However, the role of macrophage-miR-147 in atherosclerosis is yet unknown. To study that, we generated a mouse line
with a deletion of the miR-147 gene in myeloid cell line, Apoe-/-LysMcreMir147flox/flox (M-Mir147-/-), and together with
Apoe-/-LysMcreMir147+/+ (M-Mir147+/+) mice fed them a high cholesterol diet (HCD) for 12 wks. miR-147 deficiency in
macrophages increased atherosclerosis in M-Mir147-/- versus M-Mir147+/+ mice. The increased lesion size was associated
with enlarged necrotic core area, increased lesional macrophage content, increased cell death, and impaired clearance of
apoptotic cells by macrophages. The effects of miR-147 deletion on proteome of inflammatory macrophages was studied by
mass spectrometry in vitro and suggests that energy metabolism and Akt/mTOR signaling are the main targets of miR-147 in
inflammatory macrophages. MiR-147 interactome was studied in inflammatory macrophages from M(tAgo2)-Mir147-/- and
M(tAgo2)-Mir147+/+ mice, which expresses a tagged Ago2 gene following Cre recombinase activity, using an in vitro tAgo2
immunoprecipitation assay followed by RNA sequencing. Integrated analysis of interactome and proteome data suggested
Tomm6, Pdk3, and Pim1 as potential targets of miR-147 in inflammatory macrophages. Our results indicate that macrophage-
miR-147 plays a protective role against atherosclerosis probably by improving macrophage function under inflammatory
condition.
Biography
Maliheh Nazari Jahantigh obtained her bachelor’s in the field of cellular and molecular biology from Shahid Chamran University, Iran and master’s Degrees in the
field of cellular and molecular biology from Isfahan university, Isfahan, Iran and was selected as an outstanding student in the country during her master studies.
She pursued her PhD in the field of Biology (2013) from RWTH Aachen University, and then started her Postdoctoral studies at Ludwig Maximillian University
Munich (LMU), Germany respectively. Currently she is a Junior Group Leader at the Institute for Cardiovascular Disease (IPEK) of LMU. She has been studying
the role of microRNAs during atherosclerosis since 2009 and has published several papers in reputed journals in this field.
Maliheh Nazari Jahantigh, J Clin Exp Cardiolog 2018, Volume 9
DOI: 10.4172/2155-9880-C10-116