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Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (Mouse mRNA)

ABSTRACT: Atherosclerosis (AS), which is a chronic inflammatory disease, is the leading cause of death worldwide. Although several miRNAs have been reported to participate in regulating the progression of AS, there is a lack of systematic study of miRNA profile in AS. We combined miRNA and mRNA array analysis to study the global miRNAs in two AS models-oxidative LDL treated human aortic endothelial cells (HAEC) and high fat diet fed ldlr W483Stop knockin mouse. Novel miRNAs were identified to function in AS through inflammation and apoptosis pathways.

ORGANISM(S): Mus musculus

PROVIDER: GSE137581 | GEO | 2020/09/22

REPOSITORIES: GEO

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Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (Mouse miRNA)

Project description:Atherosclerosis (AS), which is a chronic inflammatory disease, is the leading cause of death worldwide. Although several miRNAs have been reported to participate in regulating the progression of AS, there is a lack of systematic study of miRNA profile in AS. We combined miRNA and mRNA array analysis to study the global miRNAs in two AS models-oxidative LDL treated human aortic endothelial cells (HAEC) and high fat diet fed ldlr W483Stop knockin mouse. Novel miRNAs were identified to function in AS through inflammation and apoptosis pathways.

2020-09-22 | GSE137582 | GEO

Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (HAEC miRNA)

2020-09-22 | GSE137580 | GEO

Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (HAEC mRNA)

2020-09-22 | GSE137578 | GEO

Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (HAEC miRNA)

Project description:Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (HAEC miRNA)

| PRJNA565964 | ENA

Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (HAEC mRNA)

Project description:Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (HAEC mRNA)

| PRJNA565963 | ENA

Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (Mouse miRNA)

Project description:Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (Mouse miRNA)

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Atlas of miRNome variations in different dyslipidemic conditions: a study in C57Bl/6, Ldlr-KO, and Pcsk9-KO mice.

Project description:In this study, mice with different genotypes and fed diets with different lipid content were enrolled, aiming to set up an atlas of miRNA expression levels in different organs with a relevant role in lipid/lipoprotein metabolism. Specifically, three genotypes were investigated: C57Bl/6 mice as controls, together with mice knock-out (KO) for LDLr (low-density lipoprotein receptor) and for PCSK9 (proprotein convertase subtilisin/kexin type 9). LDLr and PCSK9 are both involved in LDL turnover, the former mediating LDL clearance [PMID: 19299327], the latter causing the degradation of the LDLr protein [PMID: 17080197]. As a result, LDLrKO mice, because of their impaired LDL catabolism, are hypercholesterolemic and prone to atherosclerosis development, particularly when fed high-fat, cholesterol-containing diets [PMID: 8349823; PMID: 8182121]. On the contrary, PCSK9KO mice, characterized by an accelerated LDL catabolism, are hypocholesterolemic and atherosclerosis resistant [PMID: 15805190]. miRNA expression was investigated in liver, intestine, aorta, white adipose tissue and brain of mice on both standard and Western diet.

2023-09-06 | GSE227578 | GEO

Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (Mouse mRNA)

Project description:Novel mirnas participate in Atherosclerosis through inflammation and apoptosis pathways (Mouse mRNA)

| PRJNA565965 | ENA

Differential microRNA response to a high-cholesterol, high-fat diet in livers of low and high LDL-C baboons

Project description:Dysregulation of microRNAs (miRNAs) expression has been implicated in molecular genetics events leading to the progression and development of atherosclerosis. We hypothesized that miRNA expression profiles differ between baboons with low and high serum low-density lipoprotein cholesterol (LDL-C) concentrations in response to diet, and that a subset of these miRNAs regulate genes relevant to dyslipidemia and risk of atherosclerosis. We generated small RNA libraries from baboons differing in their LDL-C response to dietary fat and cholesterol (low LDL-C, n = 3; high LDL-C, n = 3) using liver biopsies collected before and after a high-cholesterol, high-fat (HCHF) challenge diet. We sequenced the libraries using Next-Generation Illumina sequencing methods, analyzed the data using mirTools software and identified 517 baboon miRNAs: 490 homologous to human and 27 novel miRNAs. HCHF diet elicited expression of more miRNAs compared to baseline (chow) diet for both low and high LDL-C baboons. Seventeen miRNAs exhibited significant differential expression in response to HCHF diet in high LDL-C baboons compared to nine miRNAs in low LDL-C baboons. Putative miRNA targets were identified with TargetScan/Base tools. miRNAs significantly targeted more genes in high LDL-C baboons compared to low LDL-C responders. Further, we identified miRNA isomers and other non-coding RNAs that were differentially expressed in response to the challenge diet.Our discovery of differentially expressed baboon miRNAs and their targets is a fundamental step in understanding the role of non-coding RNAs in the modulation of dsylipidemia.

2012-07-14 | E-GEOD-37249 | biostudies-arrayexpress

Finasteride delays atherosclerosis progression in mice and is associated with a reduction in plasma cholesterol in men

Project description:Finasteride is commonly prescribed to treat benign prostate hyperplasia and male-pattern baldness in cis men and, more recently, trans individuals. However, the effect of finasteride on cardiovascular disease remains elusive. We evaluated the role of finasteride on atherosclerosis using low-density lipoprotein (LDL) receptor-deficient (Ldlr-/-) mice. Next, we examined the relevance to humans by analysing the data deposited between 2009 and 2016 in the National Health and Nutrition Examination Survey (NHANES). We show that finasteride reduces total plasma cholesterol and delays the development of atherosclerosis in Ldlr-/- mice. Finasteride reduced monocytosis, monocyte recruitment to the lesion, macrophage lesion content, and necrotic core area, the latter of which is an indicator of plaque vulnerability in humans. RNA sequencing analysis revealed a downregulation of inflammatory pathways and an upregulation of bile acid metabolism, oxidative phosphorylation, and cholesterol pathways in the liver of mice taking finasteride. Men reporting the use of finasteride showed lower plasma levels of cholesterol and LDL-cholesterol than those not taking the drug. Our data unveil finasteride as a potential treatment to delay cardiovascular disease in people by improving the plasma lipid profile.

2024-03-06 | GSE255708 | GEO

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