RGD Reference Report - Rapidly increased neuronal mitochondrial biogenesis after hypoxic-ischemic brain injury. - Rat Genome Database

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Rapidly increased neuronal mitochondrial biogenesis after hypoxic-ischemic brain injury.

Authors: Yin, W  Signore, AP  Iwai, M  Cao, G  Gao, Y  Chen, J 
Citation: Yin W, etal., Stroke. 2008 Nov;39(11):3057-63. Epub 2008 Aug 21.
RGD ID: 2302400
Pubmed: PMID:18723421   (View Abstract at PubMed)
PMCID: PMC2726706   (View Article at PubMed Central)
DOI: DOI:10.1161/STROKEAHA.108.520114   (Journal Full-text)

BACKGROUND AND PURPOSE: Mitochondrial biogenesis is regulated through the coordinated actions of both nuclear and mitochondrial genomes to ensure that the organelles are replenished on a regular basis. This highly regulated process has been well defined in skeletal and heart muscle, but its role in neuronal cells, particularly when under stress or injury, is not well understood. In this study, we report for the first time rapidly increased mitochondrial biogenesis in a rat model of neonatal hypoxic/ischemic brain injury (H-I). METHODS: Postnatal day 7 rats were subjected to H-I induced by unilateral carotid artery ligation followed by 2.5 hours of hypoxia. The relative amount of brain mitochondrial DNA (mtDNA) was measured semiquantitatively using long fragment PCR at various time points after H-I. HSP60 and COXIV proteins were detected by Western blot. Expression of three genes critical for the transcriptional regulation of mitochondrial biogenesis, peroxisome proliferator-activated receptor coactivator-1 (PGC-1), nuclear respiratory factor-1 (NRF-1), and mitochondrial transcription factor A (TFAM), were examined by Western blot and RT-PCR. RESULTS: Brain mtDNA content was markedly increased 6 hours after H-I, and continued to increase up to 24 hours after H-I. Paralleling the temporal change in mtDNA content, mitochondrial number and proteins HSP60 and COXIV, and citrate synthase activity were increased in neurons in the cortical infarct border zone after H-I. Moreover, cortical expression of NRF-1 and TFAM were increased 6 to 24 hours after H-I, whereas PGC-1 was not changed. CONCLUSIONS: Neonatal H-I brain injury rapidly induces mitochondrial biogenesis, which may constitute a novel component of the endogenous repair mechanisms of the brain.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Brain Hypoxia-Ischemia  ISONrf1 (Rattus norvegicus)2302400; 2302400mRNA and protein:increase expression:cerebral cortexRGD 
Brain Hypoxia-Ischemia  IEP 2302400mRNA and protein:increase expression:cerebral cortexRGD 
Brain Hypoxia-Ischemia  ISOTfam (Rattus norvegicus)2302400; 2302400mRNA:increased expression:cerebral cortexRGD 
Brain Hypoxia-Ischemia  IEP 2302400mRNA:increased expression:cerebral cortexRGD 

Objects Annotated

Genes (Rattus norvegicus)
Nrf1  (nuclear respiratory factor 1)
Tfam  (transcription factor A, mitochondrial)

Genes (Mus musculus)
Nrf1  (nuclear respiratory factor 1)
Tfam  (transcription factor A, mitochondrial)

Genes (Homo sapiens)
NRF1  (nuclear respiratory factor 1)
TFAM  (transcription factor A, mitochondrial)


Additional Information