Gene expression profiling of the retinal microvessels and the brain microvessels
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ABSTRACT:
PROVIDER: PRJNA434237 | ENA |
REPOSITORIES: ENA
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Project description:Rat retinal microvessels (RMVs) and brain microvessels (BMVs) were mechanically isolated under ice-cold condition. Retinal and brain tissues (RT, BT) from the same animals were collected for comparisons. Total RNA were individually extracted, amplified and processed on Affymetrix rat 2.0 microarray Chips. We sought to obtain the whole gene expression profile of RMVs, RT, BMVs and BT. Differently expressed genes (DEGs) between RMVs and RT, and between RMVs and BMVs, between RT and BT were analyses. Using these DEGs, we comprehensively analyzed gene expression of the microvessels and highlighted their involvement in critical functional structures in RMVs and BMVs, such as junctional complex, transporters and signaling pathways.
2019-10-16 | GSE110675 | GEO
Project description:Retinal microvessels (RMVs) and brain microvessels (BMVs) were isolated from diabetic and nondiabetic rats. RNA were extracted, amplified and processed on Affymetrix rat 2.0 microarray Chips. Differently expressed genes (DEGs) between diabetic RMVs and nondiabetic RMVs, and between diabetic BMVs and nondiabetic BMVs were analyzed. Using these DEGs, we analyzed and compared the diabetic effects on the gene expression profiles in retinal microvasculature and brain microvasculature. In the brain microvasculature multiple compensatory mechanisms exists, serving to protect brain tissue from diabetic insults, whereas these mechanisms are not activated in the retinal microvasculature.
2020-03-31 | GSE113686 | GEO
Project description:A filtration method followed by microarray analyses allows PDE components to be identified in brain microvessels, and confirmed that PDE4D and PDE5A are the primary forms expressed in rat brain microvessels. Adult male F344 rats were sacrificed and blocks of the cerebral cortex and infratentorial areas were dissected. Microvessels were isolated using a filtration method, and total RNA was extracted. Two microarrays using four sample RNAs (microvessels from the cerebral cortex vs. microvessels from the infratentorial block) were included in the present study. Microarrays demonstrated that there were 16 PDE transcripts in the PDE superfamily, exhibiting quantifiable density in the microvessels.
2012-02-01 | E-GEOD-35285 | biostudies-arrayexpress
Project description:A filtration method followed by microarray analyses allows PDE components to be identified in brain microvessels, and confirmed that PDE4D and PDE5A are the primary forms expressed in rat brain microvessels.
2012-02-01 | GSE35285 | GEO
Project description:Enriched forebrain microvessels from P5, P10 and adult mice. Transcript comparisons identified 5873 genes with FC>2 between ages and 93 pathways. The observations were confronted to proteome study using NanoLS-MS/MS and deposited on proteomeXchange platform under # PXD001718. The 2 techniques converge towards extracellular matrix, cell adhesion and junction pathways, indicating early changes in development. The difference are examined as putative structural basis of very preterm intracerbral hemorrhage, 3 age comparisons of 5 days, 10 days and adult brain microvessels, 2 replicates, Agilent Whole Mouse Genome Oligo 4Ã44K Microarray
2016-01-10 | E-GEOD-67870 | biostudies-arrayexpress
Project description:Brain microvessels form the blood-brain barrier, and are dysfunctional in several neurological disorders. Brain microvessels are formed by brain microvascular endothelial cells (BMECs) and pericytes, and the molecular constituents of these cell types remain incompletely characterized, especially in humans. To improve molecular knowledge of these cell types and identify species differences in gene expression, we performed RNA-sequencing on brain microvessels isolated from human and mouse tissue samples using laser capture microdissection. We also performed RNA-sequencing of matched whole brain samples to identify genes with microvessel-enriched expression.
2020-07-23 | GSE142209 | GEO
Project description:Evaluation of early transcriptional changes in blood brain barrier genes involved in the patogenesis of brain edema associated with ALF. Two different well stablished rat models were analyzed: Portacaval anastomosis plus hepatic artery ligation and portacaval anastomosis plus total hepatectomy. ALF was induced by portocaval anastomosis (PCA) and 24 hours after the surgery animals underwent hepatic artery ligation (HAL) or total hepatectomy (HEP). Sham rats were subjected to a fictitious two-step surgery. Between 8 and 12 hours after the last surgery rats were euthanized by decapitation, to avoid anesthetic effects, and cortical microvessels isolated.
2016-04-05 | E-GEOD-79906 | biostudies-arrayexpress
Project description:Sequestration of Plasmodium falciparum-infected erythrocytes (IEs) in the brain microcirculation is a hallmark of cerebral malaria (CM), leading to endothelial activation, microvascular occlusion, brain swelling, and death. The inflammatory pathogenesis is however poorly understood, partly due to the lack of suitable in vitro platforms to study CM biology. Here, we used 3D perfusable brain microvessels to investigate combinatorial pathogen and host inflammatory stimuli over the in situ parasite maturation and IE rupture. Whereas tumor necros factor (TNF) potently upregulated adhesion molecules and inflammatory pathways, and uniformly recruited leukocytes throughout the microvessels, P. falciparum-IEs upregulated unique stress response pathways, induced minor junctional disturbances and low levels of endothelial apoptosis, and preferentially recruited leukocytes at IE binding regions. Furthermore, parasites delayed recovery from TNF stimulation and enhanced inflammatory responses. Our findings offer insights into CM biology, and suggest that multiple events intersect to promote brain barrier inflammation in CM.
2023-09-30 | GSE227672 | GEO
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.
2016-01-04 | PXD001718 | Pride
Project description:We sought to identify differentially expressed genes in several animal models of a retinal disease exhibiting vascular abnormalities and/or angiogenesis compared to control animals. Retinal microvessels were isolated from three models (RD1, Grhl3ct (Curlytail), VLDLR knock-out) and one rat model (RCS dystrophic rat), as well as from C57BL/J6 mice and non-dystrophic RCS rats as controls. Animals were used at ages appropriate to the age of vascular change of each model. Microvessels were isolated from the retinas and RNA was extracted and used in the microarray.
2013-09-13 | E-MEXP-3323 | biostudies-arrayexpress