PXD001718

PXD001718 is an original dataset announced via ProteomeXchange.

Title	Brain microvessels onotogeny-INSERM ERI28
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.
HostingRepository	PRIDE
AnnounceDate	2016-01-04
AnnouncementXML	Submission_2016-02-22_03:44:08.xml
DigitalObjectIdentifier	https://dx.doi.org/10.6019/PXD001718
ReviewLevel	Peer-reviewed dataset
DatasetOrigin	Original dataset
RepositorySupport	Supported dataset by repository
PrimarySubmitter	Philippe LEROUX
SpeciesList	scientific name: Mus musculus (Mouse); NCBI TaxID: 10090;
ModificationList	No PTMs are included in the dataset
Instrument	LTQ Orbitrap Elite

Revision	Datetime	Status	ChangeLog Entry
0	2015-01-21 07:47:09	ID requested
1	2016-01-04 03:23:30	announced
⏵ 2	2016-02-22 03:44:09	announced	Updated publication reference for PubMed record(s): 26873886.

Porte B, Hardouin J, Zerdoumi Y, Derambure C, Hauchecorne M, Dupre N, Obry A, Lequerre T, Bekri S, Gonzalez B, Flaman JM, Marret S, Cosette P, Leroux P, Major remodeling of brain microvessels during neonatal period in the mouse: A proteomic and transcriptomic study. J Cereb Blood Flow Metab, 37(2):495-513(2017) [pubmed]

submitter keyword: mouse, brain, microvessels, development, neonate, LTQ-Orbitrap

Dr Bruno Gonzalez
contact affiliation	NeoVasc; Microvascularendothelium and neonatal acquired cerebral lesions Laboratory INSERM-ER28 Faculty of Medicine and Pharmacy University of Rouen, 22 Boulevard Gambetta 76183, Rouen cedex France
contact email	bruno.gonzalez@univ-rouen.fr
lab head
Philippe LEROUX
contact affiliation	INSERM-ERI28
contact email	philippe.leroux@univ-rouen.fr
dataset submitter

Dataset FTP location NOTE: Most web browsers have now discontinued native support for FTP access within the browser window. But you can usually install another FTP app (we recommend FileZilla) and configure your browser to launch the external application when you click on this FTP link. Or otherwise, launch an app that supports FTP (like FileZilla) and use this address: ftp://ftp.pride.ebi.ac.uk/pride/data/archive/2016/01/PXD001718

PRIDE project URI

• PRIDE
  1. PXD001718
     1. Label: PRIDE project
     2. Name: Brain microvessels onotogeny-INSERM ERI28