Dataset Information

A microarray whole-genome gene expression dataset in a rat model of inflammatory corneal angiogenesis.

ABSTRACT: In angiogenesis with concurrent inflammation, many pathways are activated, some linked to VEGF and others largely VEGF-independent. Pathways involving inflammatory mediators, chemokines, and micro-RNAs may play important roles in maintaining a pro-angiogenic environment or mediating angiogenic regression. Here, we describe a gene expression dataset to facilitate exploration of pro-angiogenic, pro-inflammatory, and remodelling/normalization-associated genes during both an active capillary sprouting phase, and in the restoration of an avascular phenotype. The dataset was generated by microarray analysis of the whole transcriptome in a rat model of suture-induced inflammatory corneal neovascularisation. Regions of active capillary sprout growth or regression in the cornea were harvested and total RNA extracted from four biological replicates per group. High quality RNA was obtained for gene expression analysis using microarrays. Fold change of selected genes was validated by qPCR, and protein expression was evaluated by immunohistochemistry. We provide a gene expression dataset that may be re-used to investigate corneal neovascularisation, and may also have implications in other contexts of inflammation-mediated angiogenesis.

SUBMITTER: Mukwaya A

PROVIDER: S-EPMC5119432 | biostudies-literature | 2016 Nov

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

A microarray whole-genome gene expression dataset in a rat model of inflammatory corneal angiogenesis.

Mukwaya Anthony A Lindvall Jessica M JM Xeroudaki Maria M Peebo Beatrice B Ali Zaheer Z Lennikov Anton A Jensen Lasse Dahl Ejby LD Lagali Neil N

Scientific data 20161122

In angiogenesis with concurrent inflammation, many pathways are activated, some linked to VEGF and others largely VEGF-independent. Pathways involving inflammatory mediators, chemokines, and micro-RNAs may play important roles in maintaining a pro-angiogenic environment or mediating angiogenic regression. Here, we describe a gene expression dataset to facilitate exploration of pro-angiogenic, pro-inflammatory, and remodelling/normalization-associated genes during both an active capillary sprouti ...[more]

PMID: 27874850

Similar Datasets

Project description:Prader-Willi syndrome (PWS) is caused by loss of paternally expressed genes in the 15q11-q13 region. To further characterize alterations in gene expression in this classical obesity syndrome we used whole genome microarrays to study a PWS mouse model resulting from a paternally derived imprinting center (IC) deletion (PWS IC deletion). These mice die generally within 2-3 days of life (reflective of failure to thrive in infants with PWS) and therefore, the analysis was performed on RNA extracted from the whole brain of PWS IC deletion mice and normal littermates at less than 24 hr after birth. Of more than 45,000 probes examined, 26,471 (59%) were detected for further analysis, and 69 had a significant change in expression of at least 1.5-fold and a false discovery rate (FDR) of 5%. Eight of the genes with differential expression were imprinted and from the PWS critical region (PWSCR). The three genes with the highest expression in the PWS IC mice were pro-opiomelanocortin (Pomc) and two transcripts of unknown function. Pomc knockout mice have been shown to develop obesity. Therefore, elevated Pomc RNA in PWS IC deletion neonatal mice may be an important genetic factor in the survival of these mice as it may affect eating behavior. Interestingly, Mc5r, a melanocortin receptor known to directly respond to Pomc expression changes, was upregulated as well. Mc5r is known to be involved with thermoregulation which is reportedly abnormal in PWS infants. These observations support a role for Pomc and the network of genes involved in regulating energy homeostasis in the early clinical findings of failure to thrive observed in PWS. Other notable patterns include three previously unstudied transcripts that are expressed only from the paternal allele under regulatory control of the IC and include AK013560, BB3144814, and BB182944 (whose genes are located in the mouse PWSCR on chromosome 7B). As expected, all the known paternally expressed genes from the PWSCR had detection signals below the threshold in the PWS IC deletion mice but were clearly detectable in control littermates. Several of the genes in this study were further examined by quantitative reverse transcription-PCR (RT-PCR) to confirm their expression status. Further analysis of gene expression in these mice may lead to novel pathways affected in PWS. These results, along with other recent reports, suggest that the cumulative effect of modest changes in expression of many genes, especially genes involved in energy metabolism, contribute to the failure to thrive of infants with PWS.

Project description:PURPOSE:Fragile X syndrome, the most common inherited form of human mental retardation, arises as a consequence of a large expansion of a CGG trinucleotide repeat in 5' untranslated region of the fragile X mental retardation 1 (FMR1) gene located on the X chromosome. Although the FMR1 gene was cloned 15 years ago, the mechanisms that cause fragile X syndrome remain to be elucidated. Multiple studies have identified proteins that potentially interact with FMRP, the product of FMR1, and differentially expressed genes in an Fmr1 knockout mouse. To assess the impact of fragile X syndrome on gene expression in humans and to attempt to identify disturbed genes and gene interactive pathways relevant to fragile X syndrome, we performed gene expression microarray analysis using RNA isolated from lymphoblastoid cells derived from males with fragile X syndrome with and similarly aged control males. METHODS:We used whole genome microarrays consisting of 57,000 probes to analyze global changes to the transcriptome in readily available lymphoblastoid cell lines derived from males with fragile X syndrome and healthy comparison males with normal intelligence. We verified the differential expression of several of these genes with known biological function relevant to fragile X syndrome using quantitative reverse transcription polymerase chain reaction using RNA from lymphoblastoid cells from fragile X syndrome and control males as well as RNA from human brain tissue (frontal cortex) of other affected fragile X syndrome males. RESULTS:We identified more than 90 genes that had significant differences in probe intensity of at least 1.5-fold with a false discovery rate of 5% in cells from males with fragile X syndrome relative to comparison males. The list of 90 differentially expressed genes contained an overrepresentation of genes involved in signaling (e.g., UNC13B [-3.3-fold change in expression in lymphoblasts by quantitative reverse transcription polymerase chain reaction), GABRD [+2.0-fold change] EEF1A2 [+4.3-fold change]), morphogenesis (e.g., MAP1B [-7.5-fold change], ACCN1 [-8.0-fold change]), and neurodevelopment and function (e.g., PPP1R9B [+3.5-fold change], HES1 [+2.8-fold change]). CONCLUSIONS:These genes may represent members of candidate networks disturbed by the loss of FMR1 and consequently fragile X mental retardation protein function, thus lending support for altered fragile X mental retardation protein function resulting in an abnormal transcriptome. Further analyses of the genes, especially those that have been identified in multiple studies, are warranted to develop a more integrated description of the alterations in gene processing that lead to fragile X syndrome.

Dataset Information

A microarray whole-genome gene expression dataset in a rat model of inflammatory corneal angiogenesis.

Publications

A microarray whole-genome gene expression dataset in a rat model of inflammatory corneal angiogenesis.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets