MicroRNA miR-29c down-regulation leading to de-repression of its target DNA methyltransferase 3a promotes ischemic brain damage

Recent studies showed that stroke extensively alters cerebral microRNA (miRNA) expression profiles and several miRNAs play a role in mediating ischemic pathophysiology. We currently evaluated the significance of miR-29c, a highly expressed miRNA in rodent brain that was significantly down-regulated...

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Bibliographic Details
Published in:PloS one 2013-03, Vol.8 (3), p.e58039-e58039
Main Authors: Pandi, Gopal, Nakka, Venkata P, Dharap, Ashutosh, Roopra, Avtar, Vemuganti, Raghu
Format: Article
Language:English
Subjects:
3' Untranslated regions
Animals
Base Pairing
Base Sequence
Binding sites
Bioinformatics
Biology
Brain
Brain damage
Brain Infarction - genetics
Brain Infarction - pathology
Brain injury
Brain Ischemia - genetics
Brain Ischemia - metabolism
Brain Ischemia - pathology
Carotid arteries
Cell death
Cell Death - genetics
Cell Line
Cloning
Control
Deoxyribonucleic acid
Deprivation
Disease Models, Animal
DNA
DNA (Cytosine-5-)-Methyltransferases - genetics
DNA (Cytosine-5-)-Methyltransferases - metabolism
DNA methyltransferase
Gene expression
Gene Expression Regulation
Glucose
Hypertension
Infection
Ischemia
Laboratory animals
Male
Medicine
Metabolism
Methyltransferases
MicroRNA
MicroRNAs
MicroRNAs - genetics
MicroRNAs - metabolism
miRNA
Molecular biology
Mortality
Neurosciences
Oxygen
Pheochromocytoma cells
Prevention
Promoter Regions, Genetic
Rats
Regulations
Rest
Ribonucleic acid
RNA
RNA Interference
Rodents
siRNA
Stroke
Surgery
Transcription (Genetics)
Transcription factors
Transfection
Veins & arteries
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Summary:Recent studies showed that stroke extensively alters cerebral microRNA (miRNA) expression profiles and several miRNAs play a role in mediating ischemic pathophysiology. We currently evaluated the significance of miR-29c, a highly expressed miRNA in rodent brain that was significantly down-regulated after focal ischemia in adult rats as well as after oxygen-glucose deprivation in PC12 cells. Bioinformatics indicated that DNA methyltransferase 3a (DNMT3a) is a major target of miR-29c and co-transfection with premiR-29c prevented DNMT3a 3'UTR vector expression. In PC12 cells, treatment with premiR-29c prevented OGD-induced cell death (by 58 ± 6%; p
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0058039