Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Expression data from rat (Sprague Dawley) brain subjected to MCAo.

ABSTRACT: Middle cerebral artery occlusion (MCAo) in rat represent the ischemic stroke in human. Rodents subjected to MCAo and treated with venom phospholipase A2 showed reduction in infarct volume after 24hours of stroke. We studied the global gene expression of the reduction in infarct volume using Affymetrix Gene Chips. We analysed all the genes that were up or down regulated in the study. Total RNA isolated from sham, MCAo and MCAo+nPLA rat brains, was pooled to minimize inter-individual variation and hybridized to each array of the RAE-230A or U34A GeneChipTM according to protocols described in the GeneChipTM expression analysis package (Affymetrix, CA).

ORGANISM(S): Rattus norvegicus

SUBMITTER: Kandiah Jeyaseelan

PROVIDER: E-GEOD-17929 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

A secretory phospholipase A2-mediated neuroprotection and anti-apoptosis.

Armugam Arunmozhiarasi A Cher Charmian D N CD Lim KaiYing K Koh Dawn C I DC Howells David W DW Jeyaseelan Kandiah K

BMC neuroscience 20090923

<h4>Background</h4>Phospholipase A2 liberates free fatty acids and lysophospholipids upon hydrolysis of phospholipids and these products are often associated with detrimental effects such as inflammation and cerebral ischemia. The neuroprotective effect of neutral phospholipase from snake venom has been investigated.<h4>Results</h4>A neutral anticoagulant secretory phospholipase A2 (nPLA) from the venom of Naja sputatrix (Malayan spitting cobra) has been found to reduce infarct volume in rats su ...[more]

PMID: 19775433

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Project description:We investigated the effects of PACAP treatment, and endogenous PACAP deficiency, on infarct volume, neurological function, and the cerebrocortical transcriptional response in a mouse model of stroke, middle cerebral artery occlusion (MCAO). PACAP-38 administered i.v. or i.c.v. one hour after MCAO significantly reduced infarct volume, and ameliorated functional motor deficits measured 24 hours later in wild-type mice. Infarct volumes and neurological deficits (walking faults) were both greater in PACAP-deficient than in wild-type mice, but treatment with PACAP reduced lesion volume and neurological deficits in PACAP-deficient mice to the same level of improvement as in wild-type mice. A 35,546-clone mouse cDNA microarray was used to investigate cortical transcriptional changes associated with cerebral ischemia in wild-type and PACAP-deficient mice, and with PACAP treatment after MCAO in wild-type mice. 229 known (named) transcripts were increased (228) or decreased (1) in abundance at least 50% following cerebral ischemia in wild-type mice. 49 transcripts were significantly up-regulated only at one hour post-MCAO (acute response transcripts), 142 were up-regulated only at 24 hours post-MCAO (delayed response transcripts) and 37 transcripts were up-regulated at both times (sustained response transcripts). More than 50% of these are transcripts not previously reported to be associated with brain ischemia responses. Many of the acutely regulated neurotrauma-associated transcripts, but a larger percentage of the delayed ones, require endogenous PACAP for up-regulation by ischemia, suggesting a more prominent role for PACAP in later response to injury than in the initial response, and consistent with a neuroprotective role for PACAP in late response to injury and neuroprotective efficacy when given post-MCAO. Putative injury effector transcripts regulated by PACAP include ãÑ-actin, midline 2, and metallothionein 1. Potential neuroprotective transcripts include several demonstrated to be PACAP-regulated in other contexts. Prominent among these were transcripts encoding the PACAP-regulated gene Ier3, and the neuropeptides enkephalin, substance P (tachykinin 1), and neurotensin. Keywords: transcript identification design

Dataset Information

Expression data from rat (Sprague Dawley) brain subjected to MCAo.

Publications

A secretory phospholipase A2-mediated neuroprotection and anti-apoptosis.

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