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SRP093647
Mus musculus
24 Downloadable Samples
Illumina HiSeq 1000
Description
This dataset describe the transcriptomic profiling of cecum, stomach and ileum from wild type, cdx2 conditional knock out and cdx2 ; apc deficient mice, by mRNA-seq. Each condition was analyzed in triplicated experiment to analyze the role of cdx2 in colorectal cancer susceptibilities Overall design: Biological samples from dissected tissue were tested by RNASeq in triplicates resulting into a total of 24 samples.
Publication Title
The Cdx2 homeobox gene suppresses intestinal tumorigenesis through non-cell-autonomous mechanisms.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Homo sapiens
- 14 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Transcriptional profiles of human CD34+ cells cultured in EPO and EST conditions.
Publication Title
Cytokine-mediated increases in fetal hemoglobin are associated with globin gene histone modification and transcription factor reprogramming.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 40 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Genome wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) associated with diseases of the colon including inflammatory bowel diseases (IBD) and colorectal cancer (CRC). However, the functional role of many of these SNPs is largely unknown and tissue-specific resources are lacking. Expression quantitative trait loci (eQTL) mapping identifies target genes of disease-associated SNPs. Here, we comprehensively map eQTLs in the human colon, assess their relevance for GWAS of colonic diseases and provide functional characterization.
Publication Title
Enrichment of inflammatory bowel disease and colorectal cancer risk variants in colon expression quantitative trait loci.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HiSeq 4000
Description
RNA sequencing of human dermal fibroblasts from CAID patients passage 8 and passage 14 Overall design: RNA sequencing was perfomed on 3 wild type controls and 3 CAID patients fibroblast cell lines at cell passages 8 and 14. Sequencing was performed on Illumina Hiseq4000, 8 samples/lanes, paired-end.
Publication Title
Molecular Signature of CAID Syndrome: Noncanonical Roles of SGO1 in Regulation of TGF-β Signaling and Epigenomics.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 80 Downloadable Samples
- Illumina HiSeq 2500
Description
Aging is a major risk factor for many neurological pathologies, including Alzheimer's disease (AD). However, the mechanisms underlying brain aging and cognitive decline remain elusive. Body tissues are perfused by interstitial fluid (ISF), which is locally reabsorbed via the lymphatic vascular network. In contrast, the parenchyma of the central nervous system (CNS) is devoid of lymphatic vasculature; in the brain, removal of cellular debris and toxic molecules, such as amyloid beta (A?) peptides, is mediated by a combination of transcellular mechanisms of transport across the blood-brain and blood-cerebrospinal fluid (CSF) barriers, phagocytosis and digestion by resident microglia and recruited monocytes/macrophages, and CSF influx and ISF efflux through a paravascular route. The recent characterization of meningeal lymphatic vessels prompted a reassessment of the conventional pathways of CNS waste clearance. The role of this vasculature in brain function, specifically in the context of aging and AD, is still poorly understood. Here we show that meningeal lymphatic vessels play an essential role in maintaining brain homeostasis by draining macromolecules from the CNS (CSF and ISF) into the cervical lymph nodes. Using pharmacological, surgical, and genetic models we show that impairment of meningeal lymphatic function in adult mice slows paravascular influx of CSF macromolecules and efflux of ISF macromolecules, and induces cognitive impairment. Treatment with a lymphangiogenic factor, vascular endothelial growth factor C (VEGF-C), enhances meningeal lymphatic drainage of CSF macromolecules, improving brain perfusion and learning and memory performance in aged mice. Disruption of meningeal lymphatic vessels in transgenic mouse models of AD promotes amyloid deposition in the meninges, which closely correlates with human meningeal pathology, and aggravates overall disease severity. Our findings suggest that meningeal lymphatic dysfunction may be an aggravating factor in AD pathology and in age-associated cognitive decline. Thus, augmentation of meningeal lymphatic function might be a promising therapeutic target for preventing or delaying age-associated neurological diseases. Overall design: Male C57BL/6J mice (2 months-old) were injected (intra-cisterna magna) with Visudyne (verteporfin for injection), or vehicle as control, and submitted to a step of photoconversion, to induce meningeal lymphatic vessel ablation. This procedure was repeated 2 weeks later to ensure prolonged meningeal lymphatic dysfunction. 2 weeks after the last surgical procedure, mice were subjected to the MWM test. 3 days after, whole hippocampus was macrodissected and total RNA was extracted for sequencing.
Publication Title
Functional aspects of meningeal lymphatics in ageing and Alzheimer's disease.
Sample Metadata Fields
Age, Specimen part, Cell line, Treatment, Subject
View Samples- Mus musculus
- 80 Downloadable Samples
- Illumina HiSeq 2500
Description
Aging is a major risk factor for many neurological pathologies, including Alzheimer's disease (AD). However, the mechanisms underlying brain aging and cognitive decline remain elusive. Body tissues are perfused by interstitial fluid (ISF), which is locally reabsorbed via the lymphatic vascular network. In contrast, the parenchyma of the central nervous system (CNS) is devoid of lymphatic vasculature; in the brain, removal of cellular debris and toxic molecules, such as amyloid beta (A?) peptides, is mediated by a combination of transcellular mechanisms of transport across the blood-brain and blood-cerebrospinal fluid (CSF) barriers, phagocytosis and digestion by resident microglia and recruited monocytes/macrophages, and CSF influx and ISF efflux through a paravascular route. The recent characterization of meningeal lymphatic vessels prompted a reassessment of the conventional pathways of CNS waste clearance. The role of this vasculature in brain function, specifically in the context of aging and AD, is still poorly understood. Here we show that meningeal lymphatic vessels play an essential role in maintaining brain homeostasis by draining macromolecules from the CNS (CSF and ISF) into the cervical lymph nodes. Using pharmacological, surgical, and genetic models we show that impairment of meningeal lymphatic function in adult mice slows paravascular influx of CSF macromolecules and efflux of ISF macromolecules, and induces cognitive impairment. Treatment with a lymphangiogenic factor, vascular endothelial growth factor C (VEGF-C), enhances meningeal lymphatic drainage of CSF macromolecules, improving brain perfusion and learning and memory performance in aged mice. Disruption of meningeal lymphatic vessels in transgenic mouse models of AD promotes amyloid deposition in the meninges, which closely correlates with human meningeal pathology, and aggravates overall disease severity. Our findings suggest that meningeal lymphatic dysfunction may be an aggravating factor in AD pathology and in age-associated cognitive decline. Thus, augmentation of meningeal lymphatic function might be a promising therapeutic target for preventing or delaying age-associated neurological diseases. Overall design: Male C57BL/6J mice (2 months-old) were injected (intra-cisterna magna) with Visudyne (verteporfin for injection), or vehicle as control, and submitted to a step of photoconversion, to induce meningeal lymphatic vessel ablation. This procedure was repeated 2 weeks later to ensure prolonged meningeal lymphatic dysfunction. 2 weeks after the last surgical procedure, whole hippocampus was macrodissected and total RNA was extracted for sequencing.
Publication Title
Functional aspects of meningeal lymphatics in ageing and Alzheimer's disease.
Sample Metadata Fields
Age, Specimen part, Cell line, Treatment, Subject
View Samples- Mus musculus
- 48 Downloadable Samples
- Illumina HiSeq 2500
Description
Aging is a major risk factor for many neurological pathologies, including Alzheimer's disease (AD). However, the mechanisms underlying brain aging and cognitive decline remain elusive. Body tissues are perfused by interstitial fluid (ISF), which is locally reabsorbed via the lymphatic vascular network. In contrast, the parenchyma of the central nervous system (CNS) is devoid of lymphatic vasculature; in the brain, removal of cellular debris and toxic molecules, such as amyloid beta (A?) peptides, is mediated by a combination of transcellular mechanisms of transport across the blood-brain and blood-cerebrospinal fluid (CSF) barriers, phagocytosis and digestion by resident microglia and recruited monocytes/macrophages, and CSF influx and ISF efflux through a paravascular route. The recent characterization of meningeal lymphatic vessels prompted a reassessment of the conventional pathways of CNS waste clearance. The role of this vasculature in brain function, specifically in the context of aging and AD, is still poorly understood. Here we show that meningeal lymphatic vessels play an essential role in maintaining brain homeostasis by draining macromolecules from the CNS (CSF and ISF) into the cervical lymph nodes. Using pharmacological, surgical, and genetic models we show that impairment of meningeal lymphatic function in adult mice slows paravascular influx of CSF macromolecules and efflux of ISF macromolecules, and induces cognitive impairment. Treatment with a lymphangiogenic factor, vascular endothelial growth factor C (VEGF-C), enhances meningeal lymphatic drainage of CSF macromolecules, improving brain perfusion and learning and memory performance in aged mice. Disruption of meningeal lymphatic vessels in transgenic mouse models of AD promotes amyloid deposition in the meninges, which closely correlates with human meningeal pathology, and aggravates overall disease severity. Our findings suggest that meningeal lymphatic dysfunction may be an aggravating factor in AD pathology and in age-associated cognitive decline. Thus, augmentation of meningeal lymphatic function might be a promising therapeutic target for preventing or delaying age-associated neurological diseases. Overall design: Lymphatic endothelial cells (LECs) were isolated from meninges of adult (2-3 months-old) or old (20-24 months-old) male C57BL/6 mice. Cells were sorted by FACS according to the following phenotype: CD45-CD31+PDPN+.
Publication Title
Functional aspects of meningeal lymphatics in ageing and Alzheimer's disease.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples