Comparison of gene expression in aorta and CD115+ isolated circulating cells from apoE-/- versus apoE-/-LTbR-/- mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE63259 | GEO | 2015/03/16
SECONDARY ACCESSION(S): PRJNA267119
REPOSITORIES: GEO
Similar Datasets
Project description:Microarray gene expression profiling of aorta genes of APOE-deficient mice receiving atherosclerosis treatment with the ACE inhibitor captopril. Hypercholesterolemic APOE-deficient mice were used as a standard model of atherosclerosis to study gene expression changes during atherosclerosis treatment with the ACE inhibitor captopril. Microarray analysis was performed of whole aortas isolated from captopril-treated APOE-deficient mice relative to untreated APOE-deficient mice with overt atherosclerosis, and nontransgenic control mice. Microarray gene expression profiling revealed that captopril-mediated atherosclerosis prevention involved inhibition of aorta-infiltrating immune cells such as pro-atherogenic T lymphocytes and macrophages. Experiment Overall Design: Microarray gene expression profiling was performed of whole aortas isolated from APOE-deficient mice with atherosclerosis relative to captopril-treated APOE-deficient mice, and nontransgenic control mice. Three study groups were analyzed, i.e. 8-months-old untreated APOE-deficient mice with overt atherosclerosis, age-matched APOE-deficient mice treated for 7 months with the angiotensin-converting enzyme (ACE) inhibitor, captopril (20 mg/kg in drinking water), and nontransgenic control C57BL/6J mice. Two biological replicates were made of each group, and total RNA of three aortas was pooled for one gene chip.
2009-12-14 | E-GEOD-19286 | biostudies-arrayexpress
Project description:Lymphotoxin beta receptor (LTBR), a member of TNFRSF, was identified as a key regulator in the development, organization, and homeostasis of lymphoid tissues (Wolf, Seleznik, Zeller, & Heikenwalder, 2010). Recently, LTBR has been shown to play a role in tumor biology, both in solid tumors and in hematological cancers (Fernandes et al., 2016; Haybaeck et al., 2009; Lo et al., 2007). However, the role of LTBR in cancer biology is still controversial. From the perspective of tumor eradication, the combination of LIGHT and IFN-g can induce apoptotic cell death in HT29 cells and some other cell lines via the increase of intracellular reactive oxygen species (ROS) (Chang, Chao, Hsieh, & Lin, 2004; Zhang, Liu, Demchik, Zhai, & Yang, 2004). Artificial LTBR agonist was shown to induce tumor necrosis and decrease tumor burden in vivo in colon cancer or melanoma. (Hu et al., 2013), while recent studies revealed that LTBR mediated tumor progression, triggered by either LTα1b2 or LIGHT stimulation, leads to the recruitment of more infiltrating immune cells and the secretion of pro-survival inflammatory cyto-/chemokines (Ware, 2005). From this, the aim of the project is to compare the signalling changes between WT cells and HOIP absent Hep3B cells using a moTAP tagged LIGHT ligand. This ligand was pulled down by Flag IP, followed by Strep-tactin IP to explore the LTBR signalling complex with and without LUBAC. The result from this experiment would provide an unbiased picture of components of the LTBR-SC, also pointing out the differences between canonical NF-kB pathway and noncanonical Nf-kB pathway.
2025-04-01 | PXD034142 | Pride
Project description:The presence of high endothelial venules (HEV) and tertiary lymphoid structures (TLS) in solid tumors is correlated with favorable prognosis in many cancer types and has been associated with better treatment responses to immune-checkpoint blockade (ICB). However, the molecular mechanisms underlying intratumoral HEV and TLS formation and their contribution to anti-tumor responses remain unclear. Lymphotoxin beta receptor (LTBR) signaling is a critical regulator of lymph node organogenesis and when combined with antiangiogenic and ICB treatment can augment tumor-associated HEV formation. Here we demonstrate that LTBR signaling modulates the tumor microenvironment via multiple mechanisms to promote anti-tumor T cell responses. Systemic activation of the LTBR pathway via agonistic antibody treatment induced tumor-specific HEV formation, upregulated the expression of TLS-related chemokines, and enhanced dendritic cell (DC) and T cell infiltration and activation in syngeneic tumor models. In vitro studies confirmed direct effects of LTBR agonism on DC activation and maturation and associated DC- mediated T cell activation. Single agent LTBR agonist treatment inhibited syngeneic tumor growth in a CD8+ T cell- and HEV-dependent manner; and the LTBR agonist enhanced anti-tumor effects of anti-PD-1 and CAR T cell therapies, respectively. An in vivo tumor screen for TLS-inducing cytokines revealed that the combination of LTBR agonism and lymphotoxin alpha (LT⍺) expression promoted robust intratumoral TLS induction and enhanced tumor responses to anti-CTLA-4 treatment. Collectively, this study highlights crucial functions of LTBR signaling in modulating the tumor microenvironment and inform future HEV/TLS- based strategies for cancer treatments.
2024-08-08 | GSE243170 | GEO
Project description:Oryctolagus cuniculus LTBR, Oryctolagus cuniculus lymphotoxin beta receptor (LTBR), mRNA. [Source:RefSeq mRNA;Acc:NM_001267705], is expressed in 1 baseline experiment(s);
| ENSOCUG00000001292 | ExpressionAtlas
Project description:Inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H) exhibit a marked difference in their susceptibility to atherosclerosis and the arterial wall has proven to be a source of the difference in atherosclerosis susceptibility. Genome-wide gene expression analysis was conducted in aortic walls of the two strains. Total RNA was extracted from aortas of 6-week-old female B6 and C3H apoE-deficient (apoE-/-) mice fed a chow or Western diet. 1514 genes in chow fed mice and 590 genes in Western fed mice were found to be differentially expressed between the two strains. RNA was extracted from aorta using a Trizol protocol. Total RNA was pooled in an equal amount from 4 mice for each group. Standard Affymetrix procedures were performed using 8ug of total RNA. Microarrays were used to detect gene expression in aortic walls of two apoE-deficient mouse strains when fed a chow or western diet. Experiment Overall Design: 4 groups of mice were studied: C57BL/6 apoE-/- mice on chow diet (03-62_BC), C57BL/6 apoE-/- mice on Western diet (03-62_BW), C3H/HeJ apoE-/- mice on chow diet (03-62_CC), and C3H/HeJ apoE-/- mice on Western diet (03-62_CW). Mice were weaned at 3 weeks of age onto a chow diet. At 4 weeks of age, mice were switched onto a western diet or continued the chow diet for 2 additional weeks.
2009-02-28 | E-GEOD-14854 | biostudies-arrayexpress
Project description:Rattus norvegicus Ltbr, lymphotoxin beta receptor [Source:RGD Symbol;Acc:1309448], is expressed in 6 baseline experiment(s);
| ENSRNOG00000019264 | ExpressionAtlas
Project description:Monodelphis domestica LTBR, lymphotoxin beta receptor [Source:NCBI gene;Acc:100014805], is expressed in 2 baseline experiment(s);
| ENSMODG00000018059 | ExpressionAtlas
Project description:Rattus norvegicus Ltbr, lymphotoxin beta receptor [Source:RGD Symbol;Acc:1309448], is differentially expressed in 31 experiment(s);
| ENSRNOG00000019264 | ExpressionAtlas
Project description:Microarray gene expression profiling of aorta genes of APOE-deficient mice receiving atherosclerosis treatment with the ACE inhibitor captopril. Hypercholesterolemic APOE-deficient mice were used as a standard model of atherosclerosis to study gene expression changes during atherosclerosis treatment with the ACE inhibitor captopril. Microarray analysis was performed of whole aortas isolated from captopril-treated APOE-deficient mice relative to untreated APOE-deficient mice with overt atherosclerosis, and nontransgenic control mice. Microarray gene expression profiling revealed that captopril-mediated atherosclerosis prevention involved inhibition of aorta-infiltrating immune cells such as pro-atherogenic T lymphocytes and macrophages.
2009-12-03 | GSE19286 | GEO
Project description:Macaca mulatta LTBR, lymphotoxin beta receptor [Source:VGNC Symbol;Acc:VGNC:100075], is expressed in 2 baseline experiment(s);
| ENSMMUG00000020213 | ExpressionAtlas