Identification of differentially expressed genes induced by transient ischemic stroke
Abstract
We have used a rat model of focal cerebral ischemia to investigate changes in gene expression that occur during stroke. To monitor these changes, we employed representational difference analysis-polymerase chain reaction (PCR). A total of 128 unique gene fragments were isolated, and we selected 13 of these for quantitative reverse transcriptase-PCR analysis. Of these 13 genes, we found seven that were differentially expressed. Four of these genes have not previously been implicated in stroke, and include neuronal activity regulated pentraxin (Narp), cysteine rich protein 61 (Cyr61), Bcl-2 binding protein BIS (Bcl-2-interacting death suppressor), and lectin-like ox-LDL receptor (LOX-1). We demonstrated differential expression of each gene by quantitative PCR analysis, and in the case of LOX-1, we further confirmed differential expression by in situ hybridization. LOX-1 expression is induced greater than ten fold at the core lesion site, and is essentially localized to the ipsilateral half of the brain. LOX-1 appears to be expressed in a non-neuronal cell type, and it does not appear to be expressed in vascular endothelial cells within the brain. This suggests that LOX-1 may serve a novel function in the brain.
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Internalisation of AMPAR receptors upon TACE action may serve as a protective mechanism against excess glutamate.
“The internalisation of AMPAR receptors upon TACE action (Cho et al. 2008) may serve as a protective mechanism against the excess of glutamate (Schwarz et al. 2002).”
From Neuronal pentraxins as biomarkers of synaptic activity: from physiological functions to pathological changes in neurodegeneration (2022) · cites this paper as Schwarz et al. 2002
NPTX2 was originally described as an immediate early gene induced by seizures and stroke in the rat hippocampus, mechanisms that involved an excess of glutamate in the synaptic cleft.
“On the other hand, NPTX2 was originally described as an IEG induced by seizures and stroke in the rat hippocampus; mechanisms that involved an excess of glutamate in the synaptic cleft (Schwarz et al. 2002; Tsui et al. 1996).”
From Neuronal pentraxins as biomarkers of synaptic activity: from physiological functions to pathological changes in neurodegeneration (2022) · cites this paper as Schwarz et al. 2002
NPTX2 upregulation may promote AMPAR internalization, protecting against excitotoxicity.
“This may promote AMPAR internalization, protecting against excitotoxicity (Schwarz et al. 2002).”
From Neuronal pentraxins as biomarkers of synaptic activity: from physiological functions to pathological changes in neurodegeneration (2022) · cites this paper as Schwarz et al. 2002
NPTX2 is upregulated in a rat model of cerebral ischaemia.
“Similarly, NPTX2 was upregulated in a rat model of cerebral ischaemia.”
From Neuronal pentraxins as biomarkers of synaptic activity: from physiological functions to pathological changes in neurodegeneration (2022) · cites this paper as Schwarz et al. 2002
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- Authors
- Schwarz, D. A., Barry, G., Mackay, K. B., Manu, F., Naeve, G. S., Vana, A. M., Verge, G., Conlon, P. J., Foster, A. C., & Maki, R. A.
- Affiliations
- Neurocrine Biosciences (United States) (US)
- Corresponding author
- Schwarz, David A
- Venue
- Molecular Brain Research
- Publisher
- Elsevier BV
- Published
- 2002-05
- Volume
- 101
- Issue
- 1-2
- Pages
- 12-22
- ISSN
- 0169-328X (ISSN-L)
- OpenAlex
- W2043950289
- Cited by
- 65
- References
- 38
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 3 · 2023: 1 · 2022: 1 · 2021: 5 · 2020: 2 · 2019: 1 · 2018: 1 · 2017: 4 · 2016: 4 · 2015: 2 · 2014: 1 · 2013: 1 · 2012: 2
- FWCI
- 3.44
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Epidemiology › Acute Ischemic Stroke Management
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- transient ischemic stroke, focal cerebral ischemia, differentially expressed genes, gene expression changes, LOX-1, NARP, CYR61, rat stroke model
- MeSH terms
- Animals, Cerebral Cortex, Cerebral Infarction, Brain Ischemia, Endothelium, Vascular, Gene Expression Regulation, Male, Neuroglia, Receptors, LDL, RNA, Messenger, Reperfusion Injury, Up-Regulation, Neostriatum, Rats, Sprague-Dawley, DNA, Complementary, Stroke, Scavenger Receptors, Class E, Receptors, Oxidized LDL, Rats
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