Microarray analysis of femoral artery injury in mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Richard Assoian
PROVIDER: E-GEOD-40637 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:The whole rat genome microarray expression profiling of carotid artery specimen was emplyed to identify the gene expression profile before and after balloon injury. In our study, the neointimal formation of carotid arteries was apparent at day 7 and markedly increased at day 21 after balloon injury. In order to investigate the underlying mechanism of neointimal formationin in injured carotid arteries, all genes involved in signaling pathways whose expression was altered 2-fold in injured carotid arteries at day 7 and day 21 as compared to uninjured arteries were filtered out. Expression of four genes (TLR4, IRAK1, IM-NM-:BM-NM-1, IL-1M-NM-2) from TLR signaling pathway was quantified in the same RNA samples by quantitative real-time PCR, conforming that TLR signaling pathway participated in neointimal formation of carotid arteries after balloon injury. Balloon injury-induced gene expression in wistar rat was measured at day 7 and day 21 after balloon injury as compared with uninjured arteries. Two independent experiments were performed at each time (uninjured, day 7 or day 21) using different wistar rats for each experiment.
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Project description:The proliferation and remodeling of vascular smooth muscle cells (VSMCs) is an important pathological event in atherosclerosis and restenosis. Here we report that microRNA-132 (miR-132) blocks vascular smooth muscle cells (VSMC) proliferation by inhibiting the expression of LRRFIP1 [leucine-rich repeat (in Flightless 1) interacting protein-1]. MicroRNA microarray revealed that miR-132 was upregulated in the rat carotid artery after catheter injury, which was further confirmed by quantitative real-time RT-PCR. Transfection of an miR-132 mimic significantly inhibited the proliferation of VSMCs, whereas transfection of an miR-132 antagomir increased it. Bioinformatics showed that LRRFIP1 is a target candidate of miR-132. miR-132 down-regulated luciferase activity driven by a vector containing the 3’-untranslated region of Lrrfip1 in a sequence-specific manner. LRRFIP1 induced VSMC proliferation. Immunohistochemical analysis revealed that Lrrfip1 was clearly expressed along with the basal laminar area of smooth muscle, and its expression pattern was disrupted 7 days after arterial injury LRRFIP1 mRNA was decreased 14 days after injury. Delivery of miR-132 to rat carotid artery attenuated neointimal proliferation in carotid artery injury models. Our results suggest that miR-132 is a novel regulator of VSMC proliferation that represses neointimal formation by inhibiting LRRFIP1 expression. Balloon injury was induced in the carotid arteries of male Sprague–Dawley rats weighing approximately 250 g. Total RNA were extracted from the arterial sections after 10 days. MicroRNA profile of the sample was compared with non-injured control.
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Project description:The whole rat genome microarray expression profiling of carotid artery specimen was emplyed to identify the gene expression profile before and after balloon injury. In our study, the neointimal formation of carotid arteries was apparent at day 7 and markedly increased at day 21 after balloon injury. In order to investigate the underlying mechanism of neointimal formationin in injured carotid arteries, all genes involved in signaling pathways whose expression was altered 2-fold in injured carotid arteries at day 7 and day 21 as compared to uninjured arteries were filtered out. Expression of four genes (TLR4, IRAK1, IκBα, IL-1β) from TLR signaling pathway was quantified in the same RNA samples by quantitative real-time PCR, conforming that TLR signaling pathway participated in neointimal formation of carotid arteries after balloon injury.
2013-06-29 | GSE48279 | GEO