Reduction and restoration of mitochondrial DNA content after focal cerebral ischemia/reperfusion

Hong Chen, Chaur Jong Hu, Yong Y. He, Ding I. Yang, Jan Xu, Chung Y. Hsu

Research output: Contribution to journalArticle

61 Citations (Scopus)

Abstract

Background and Purpose - Oxidative damage of mitochondrial DNA (mtDNA) in the ischemic brain is expected after ischemia/reperfusion injury. A recent study demonstrated limited patterns of mtDNA deletion in the brain after ischemia/reperfusion. We studied the ischemia/reperfusion-induced global changes of mtDNA integrity and its restoration in a rat model of transient focal ischemia in vivo. Methods - Changes in mtDNA content in the ischemic brain were assessed with the use of a rat stroke model featuring transient severe ischemia confined to the cerebral cortex of the right middle cerebral artery territory for 30 or 90 minutes. A new long polymerase chain reaction method, using mouse DNA as an internal standard, was applied to measure the relative content of intact rat mtDNA. Southern hybridization following alkaline gel electrophoresis was conducted in a parallel study to confirm long polymerase chain reaction results. Results - A reduction in mtDNA content was found after ischemia for 30 and 90 minutes. The mtDNA was restored to near nonischemic levels 24 hours after 30- but not 90-minute ischemia. Conclusions - These results confirm that ischemia/reperfusion causes mtDNA damages. Restoration of the mtDNA content to nonischemic levels after 30-minute ischemia raises the possibility that mtDNA repair or repletion occurs after brief ischemia.

Original languageEnglish
Pages (from-to)2382-2387
Number of pages6
JournalStroke
Volume32
Issue number10
Publication statusPublished - 2001
Externally publishedYes

Fingerprint

Brain Ischemia
Mitochondrial DNA
Reperfusion
Ischemia
Polymerase Chain Reaction
Middle Cerebral Artery
Brain
Reperfusion Injury
DNA Repair
Cerebral Cortex
DNA Damage
Electrophoresis
Gels
Stroke
DNA

Keywords

  • Cerebral ischemia, focal
  • DNA damage
  • DNA repair
  • DNA, mitochondrial
  • Rats

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Neuroscience(all)

Cite this

Chen, H., Hu, C. J., He, Y. Y., Yang, D. I., Xu, J., & Hsu, C. Y. (2001). Reduction and restoration of mitochondrial DNA content after focal cerebral ischemia/reperfusion. Stroke, 32(10), 2382-2387.

Reduction and restoration of mitochondrial DNA content after focal cerebral ischemia/reperfusion. / Chen, Hong; Hu, Chaur Jong; He, Yong Y.; Yang, Ding I.; Xu, Jan; Hsu, Chung Y.

In: Stroke, Vol. 32, No. 10, 2001, p. 2382-2387.

Research output: Contribution to journalArticle

Chen, H, Hu, CJ, He, YY, Yang, DI, Xu, J & Hsu, CY 2001, 'Reduction and restoration of mitochondrial DNA content after focal cerebral ischemia/reperfusion', Stroke, vol. 32, no. 10, pp. 2382-2387.
Chen, Hong ; Hu, Chaur Jong ; He, Yong Y. ; Yang, Ding I. ; Xu, Jan ; Hsu, Chung Y. / Reduction and restoration of mitochondrial DNA content after focal cerebral ischemia/reperfusion. In: Stroke. 2001 ; Vol. 32, No. 10. pp. 2382-2387.
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AU - Hsu, Chung Y.

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N2 - Background and Purpose - Oxidative damage of mitochondrial DNA (mtDNA) in the ischemic brain is expected after ischemia/reperfusion injury. A recent study demonstrated limited patterns of mtDNA deletion in the brain after ischemia/reperfusion. We studied the ischemia/reperfusion-induced global changes of mtDNA integrity and its restoration in a rat model of transient focal ischemia in vivo. Methods - Changes in mtDNA content in the ischemic brain were assessed with the use of a rat stroke model featuring transient severe ischemia confined to the cerebral cortex of the right middle cerebral artery territory for 30 or 90 minutes. A new long polymerase chain reaction method, using mouse DNA as an internal standard, was applied to measure the relative content of intact rat mtDNA. Southern hybridization following alkaline gel electrophoresis was conducted in a parallel study to confirm long polymerase chain reaction results. Results - A reduction in mtDNA content was found after ischemia for 30 and 90 minutes. The mtDNA was restored to near nonischemic levels 24 hours after 30- but not 90-minute ischemia. Conclusions - These results confirm that ischemia/reperfusion causes mtDNA damages. Restoration of the mtDNA content to nonischemic levels after 30-minute ischemia raises the possibility that mtDNA repair or repletion occurs after brief ischemia.

AB - Background and Purpose - Oxidative damage of mitochondrial DNA (mtDNA) in the ischemic brain is expected after ischemia/reperfusion injury. A recent study demonstrated limited patterns of mtDNA deletion in the brain after ischemia/reperfusion. We studied the ischemia/reperfusion-induced global changes of mtDNA integrity and its restoration in a rat model of transient focal ischemia in vivo. Methods - Changes in mtDNA content in the ischemic brain were assessed with the use of a rat stroke model featuring transient severe ischemia confined to the cerebral cortex of the right middle cerebral artery territory for 30 or 90 minutes. A new long polymerase chain reaction method, using mouse DNA as an internal standard, was applied to measure the relative content of intact rat mtDNA. Southern hybridization following alkaline gel electrophoresis was conducted in a parallel study to confirm long polymerase chain reaction results. Results - A reduction in mtDNA content was found after ischemia for 30 and 90 minutes. The mtDNA was restored to near nonischemic levels 24 hours after 30- but not 90-minute ischemia. Conclusions - These results confirm that ischemia/reperfusion causes mtDNA damages. Restoration of the mtDNA content to nonischemic levels after 30-minute ischemia raises the possibility that mtDNA repair or repletion occurs after brief ischemia.

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