Project description:This experiment contains a subset of data from the BLUEPRINT Epigenome project ( http://www.blueprint-epigenome.eu ), which aims at producing a reference haemopoetic epigenomes for the research community. 29 samples of primary cells or cultured primary cells of different haemopoeitc lineages from cord blood are included in this experiment. This ArrayExpress record contains only meta-data. Raw data files have been archived at the European Genome-Phenome Archive (EGA, www.ebi.ac.uk/ega) by the consortium, with restricted access to protect sample donors' identity. The relevant accessions of EGA data sets is EGAD00001001165. Details on how to apply for data access via the BLUEPRINT data access committee are on the EGA data set pages. The mapping of samples to these EGA accessions can be found in the 'Sample Data Relationship Format' file of this ArrayExpress record. Information on individual samples and sequencing libraries can also be found on the BLUEPRINT data coordination centre (DCC) website: http://dcc.blueprint-epigenome.eu
Project description:This experiment contains a subset of data from the BLUEPRINT Epigenome project ( http://www.blueprint-epigenome.eu ), which aims at producing a reference haemopoetic epigenomes for the research community. 4 samples of primary cells from tonsil with cell surface markes CD20med/CD38high in young individuals (3 to 10 years old) are included in this experiment. This ArrayExpress record contains only meta-data. Raw data files have been archived at the European Genome-Phenome Archive (EGA, www.ebi.ac.uk/ega) by the consortium, with restricted access to protect sample donors' identity. The relevant accessions of EGA data sets is EGAD00001001523. Details on how to apply for data access via the BLUEPRINT data access committee are on the EGA data set pages. The mapping of samples to these EGA accessions can be found in the 'Sample Data Relationship Format' file of this ArrayExpress record. Information on individual samples and sequencing libraries can also be found on the BLUEPRINT data coordination centre (DCC) website: http://dcc.blueprint-epigenome.eu
Project description:This experiment contains a subset of data from the BLUEPRINT Epigenome project ( http://www.blueprint-epigenome.eu ), which aims at producing a reference haemopoetic epigenomes for the research community. 74 samples of primary cells or cultured primary cells of different haemopoeitc lineages from cord blood, venous blood, bone marrow and thymus are included in this experiment. This ArrayExpress record contains only meta-data. Raw data files have been archived at the European Genome-Phenome Archive (EGA, www.ebi.ac.uk/ega) by the consortium, with restricted access to protect sample donors' identity. There are 32 EGA data set accessions, which can be found under the Comment[EGA_DATA_SET] column in the 'Sample Data Relationship Format' (SDRF) file of this ArrayExpress record (http://www.ebi.ac.uk/arrayexpress/files/E-MTAB-3827/E-MTAB-3827.sdrf.txt). Details on how to apply for data access via the BLUEPRINT data access committee are on the EGA data set pages. Likewise, mapping of samples to these EGA accessions can be found in the SDRF file. Please note that the raw data files for 11 sequencing runs have yet been deposited at EGA, so they are marked with \\ot available\\ under the Comment[SUBMITTED_FILE_NAME] field in the SDRF file, and were included for the sake of completeness. Further iInformation on individual samples and sequencing libraries can also be found on the BLUEPRINT data coordination centre (DCC) website: http://dcc.blueprint-epigenome.eu\
Project description:Acquired neonatal brain lesions result from the co-incidence of environment deleterious factors occurring at a specific development stage. Hypoxia-ischemia and inflammation are the major triggers of brain damage in late pregnancy and early infancy, and result in a variety of damages depending on whether it affected fetuses, early or late preterm infants or at term neonates. Indeed brain responses to insults are different depending on age, since cerebral tissue presents a rapidly evolving cellular and biochemical substrate in this period. Clearly age-dependent etiology is largely documented; e.g. Intraventricular/intraparenchymal (IVH/IPH) brain hemorrhage in fetuses and extreme preterm (less than 28 gestation weeks; GW); focal or diffuse periventricular leucomalacia in preterm aged 28-34 GW or cortical necrosis in term infants. Definite periods of occurrence of preterm-encephalopathy are associated to particular vulnerability of distinct cell populations. Functional deficits remain in grown-up and represent a human and economical burden. IVH/IPH affects extreme preterm infants. It specific periventricular germinal matrix (GM) localization reveal vascular vulnerability at this site during a definite period. GM is the site of particularly intense metabolism due to neural cell precursor multiplication and angiogenesis. In addition, GM is at risk of hypoperfusion or perfusion arrest due to its watershed situation between centripetal and centrifugal vascular supplies, especially in very preterm infants otherwise subjected to fluctuant hemodynamics. Thus vascular bed in GM cumulates hypoxia-ischemia risks. The vulnerability of vasculature in this area was referred to be linked to intense angiogenesis and micro-vessels remodeling. Indeed endothelial support by pericytes and astrocytes end-feet is loose in these vessels and angiogenic factors also exhibit pro-hemorrhage potential. The blood to brain interface referred to as neurovascular unit is the multicellular structure shaping endothelial cells to regulate vascular permeability. The blood brain barrier (BBB) restrains pericellular diffusion and allows specific trans-endothelial transports. In previous studies in mice, we have observed structural and functional differences between young and adult brain microvascular endothelial cells (mvEC). Of note mvEC from neonates express the NMDA receptor and glutamate in these cells elicit protease secretions involved in vascular remodeling, while adult mvEC did not. Genetic inactivation of the t-PA inhibitor-1 allowed to mimick an age dependent IVH/IPH up to 5 days post-natal (P5) in mice. These observations (and others) support the hypothesis that mouse brain microvessels represent a heuristic paradigm in the study of vascular maturity as a favoring background for age dependent neonate brain hemorrhage. The present project was designed at studying constitutive protein contents of brain microvessels in a large scale, around the period of high disruption propensity (P5). We prepared enriched fractions of mouse forebrain microvessels (fMV) in order to insolating the neurovascular unit made of endothelial cells linked by blood brain barrier junctions, basal lamina including pericytes, astrocyte and neuritic end-feet from P5 (pro-hemorrhagic state), P10 (Immature hemorrhage resistant state) and P60 (Mature) mice, to study proteome onotogeny in fMV.