Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA168220 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene expression profiles from the aortic arch of Ldlr-/-Apob100/100 Mttpflox/flox Mx1-Cre mice at different stages of atherosclerosis development
2012-06-08 | GSE38574 | GEO
Project description:Gene expression profiles from the aortic arch of Ldlr-/-Apob100/100 Mttpflox/flox Mx1-Cre mice at different stages of atherosclerosis development Total RNAs from the aortic arch were collected at different time points during atherosclerosis development (10, 20, 30, 40, 50, and 60 weeks of age), 4-7 mice per time point.
2012-06-07 | E-GEOD-38574 | biostudies-arrayexpress
Project description:LRF, which is encoded by the ZBTB7A gene and formerly known as POKEMON (POK erythroid myeloid ontogenic factor), was originally identified as a PLZF (promyelocytic leukemia zinc finger) homologue interacting with BCL6 (B-cell lymphoma 6). LRF is a transcription factor that is broadly expressed in hematopoietic lineage cells, but its expression is particularly high in erythroblasts and germinal center (GC) B-cells. The goal of this study is to assess the effect of LRF loss on the LT-HSC transcriptome. Nine days after injection of adult mice with polyinosinic polycytidylic acid (pIpc) to activate Cre, total RNAs were isolated from double-sorted LT-HSCs from LRF Flox/+ Mx1-Cre+ and LRF Flox/Flox Mx1-Cre+ mice and processed for microarray analysis. We performed gene expression microarray analysis of FACS-sorted LT-HSCs (LSK IL7Ra-Flt3-CD150+CD48-) to assess the effect of Lrf loss on the LT-HSC transcriptome. Zbtb7a Flox/+ Mx1-Cre+ mice were used as a control to normalize the potential effects of Cre recombinase. LT-HSCs were FACS-sorted from three Lrf knockout (Zbtb7a Flox/Flox Mx1-Cre+) and two control (Zbtb7a Flox/+ Mx1-Cre+) mice, nine days after the first pIpC injection.
2012-10-26 | E-GEOD-41839 | biostudies-arrayexpress
Project description:We performed proteomic analyses on the kidneys of Tmod1 flox/flox/Ksp-Cre- (TF) and Tmod1 flox/flox/Ksp-Cre+ (TFK) mice.
2019-06-10 | MSV000083953 | MassIVE
Project description:We here performed a proteomics study on the colon tissues of ckmt1 KOIEC or. WT (flox+/+) mice after DSS treatment for 8 days (n=3). KOIEC mice (Ckmt1flox/flox, Vil-Cre) means mice with intestinal epithelial conditional knockout (C57BL/6J). Cre-negative Ckmt1 flox/flox littermates were used as controls. Group 1: DSSCKO (Ckmt1flox/flox, Vil-Cre) Group 2: DSSflox (Cre-negative Ckmt1 flox/flox littermates)
2025-05-07 | PXD057053 | Pride
Project description:LRF, which is encoded by the ZBTB7A gene and formerly known as POKEMON (POK erythroid myeloid ontogenic factor), was originally identified as a PLZF (promyelocytic leukemia zinc finger) homologue interacting with BCL6 (B-cell lymphoma 6). LRF is a transcription factor that is broadly expressed in hematopoietic lineage cells, but its expression is particularly high in erythroblasts and germinal center (GC) B-cells. The goal of this study is to assess the effect of LRF loss on the LT-HSC transcriptome. Nine days after injection of adult mice with polyinosinic polycytidylic acid (pIpc) to activate Cre, total RNAs were isolated from double-sorted LT-HSCs from LRF Flox/+ Mx1-Cre+ and LRF Flox/Flox Mx1-Cre+ mice and processed for microarray analysis.
2012-10-26 | GSE41839 | GEO
Project description:Analysis of the transcriptional signature of FACS-purified splenic DC subsets from Ldlr deficient mice transplanted with control or Cd11c-cre Atg16l1flox/flox bone marrow and subjected to an atherogenic diet for 8 weeks
2019-09-20 | GSE137760 | GEO
Project description:Aims: Mitochondria are involved in cellular metabolism, energy production, calcium homeostasis, sterol and bile acids (BAs) synthesis. Mitochondria are plastic organelles and continuously undergo biogenesis, fusion, fission and mitophagy. On these premises, we tested how the overexpression of OPA1, an inner mitochondrial membrane fusion protein, impacts lipids, lipoprotein metabolism and atherosclerosis development in LDL-R deficient mice (LDLR KO). Methods: OPA1TG/LDLR KO and OPA1ΔHep /LDLR KO were generated and fed with a Western-type diet (WTD) for 12 weeks. Atherosclerosis development was compared to that of LDLR KO mice. In humans, OPA1 expression was investigated in samples from 78 asymptomatic and symptomatic human subjects within the Carotid Plaque Imaging Project (CPIP). Results: OPA1TG/LDLR KO mice showed a significant increase in plasma cholesterol levels mainly in VLDL and LDL fractions. OPA1TG/LDLR KO display a reduction of unconjugated bile acids and higher percentage of conjugated bile acids leading to an increased lipid adsorption. This phenotype was associated with increased atherosclerosis in the aortic root. OPA1 overexpression affects also vascular smooth muscle cell cellular metabolism, leading to an increase in the synthetic vs the proliferative phenotype. Vice versa, hepatocyte deletion of OPA1 improved systemic lipoprotein metabolism and protected from atherosclerosis. The analysis of human atherosclerotic samples indicated that a higher OPA1 expression in the plaque is associated with a reduced degradation of extracellular matrix as well as the expression of markers of cell migration and differentiation. Conclusion: Mitochondrial fusion mediated by OPA1 plays a key role in atherosclerosis by affecting lipoprotein metabolism as well as vascular smooth muscle cell biology.
2025-10-27 | PXD060456 | Pride
Project description:OPA1 (Optic Atrophy 1), a mitochondrial inner membrane protein involved in mitochondrial cellular metabolism, energy production, calcium homeostasis, and sterol and bile acids (BAs) synthesis. Mitochondria are plastic organelles continuously undergoing biogenesis, fusion, fission, and mitophagy. On these premises, we tested how the overexpression of OPA1, an inner mitochondrial membrane fusion protein, impacts lipids, lipoprotein metabolism, and atherosclerosis development in LDL-R deficient mice (LDLR KO). Methods: OPA1TG/LDLR KO and OPA1ΔHep /LDLR KO were generated and fed with a Western-type diet (WTD) for 12 weeks. Atherosclerosis development was compared to that of LDLR KO mice. In humans, OPA1 expression was investigated in samples from 78 asymptomatic and symptomatic human subjects within the Carotid Plaque Imaging Project (CPIP). Results: OPA1TG/LDLR KO mice showed a significant increase in plasma cholesterol levels mainly in VLDL and LDL fractions. OPA1TG/LDLR KO display a reduction of unconjugated bile acids and higher percentage of conjugated bile acids leading to an increased lipid adsorption. This phenotype was associated with increased atherosclerosis in the aortic root. OPA1 overexpression affects also vascular smooth muscle cell cellular metabolism, leading to an increase in the synthetic vs the proliferative phenotype. Vice versa, hepatocyte deletion of OPA1 improved systemic lipoprotein metabolism and protected from atherosclerosis. The analysis of human atherosclerotic samples indicated that a higher OPA1 expression in the plaque is associated with a reduced degradation of extracellular matrix as well as the expression of markers of cell migration and differentiation. Conclusion: Mitochondrial fusion mediated by OPA1 plays a key role in atherosclerosis by affecting lipoprotein metabolism as well as vascular smooth muscle cell biology.
2025-10-27 | PXD060450 | Pride
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