Preconditioning with chronic cerebral hypoperfusion reduces a focal cerebral ischemic injury and increases apurinic/apyrimidinic endonuclease/redox factor-1 and matrix metalloproteinase-2 expression

Sun Ah Choi, Hee Kim Eum, Yun Lee Jong, Suck Nam Hyo, Hyun Kim Seo, Whan Kim Gyung, In Lee Byung, Jihoe Heo

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Atherosclerosis may cause severe stenosis of the arteries supplying the brain, which induces chronic cerebral hypoperfusion. Although an infarction often occurs in the chronically hypoperfused brain area, it has been uncertain whether the stroke severity is attenuated or increased when further decrease of blood flow occurs. To test the hypothesis that chronic cerebral hypoperfusion is protective against the subsequent severe ischemia, we examined the effect of chronic cerebral hypoperfusion on brains subjected to acute focal ischemia. Spontaneous hypertensive rats were subjected to middle cerebral artery occlusion/reperfusion four weeks after bilateral common carotid artery ligation (BCAL) or sham operation. The rats with BCAL had smaller infarctions, determined by 2,3,5-triphenyltetrazolium hydrochloride staining, and less severe neurologic deficits than those with sham operation. The number of DNAdamaged cells, examined by the in situ nick translation study, was significantly reduced in animals with BCAL. Immunoreactivity for apurinic/apyrimidinic endonuclease/redox factor-1, which plays a role in cellular defense mechanism, was markedly increased in those with BCAL. Indirect evidence of extracellular matrix remodeling, which might be associated with adaptive arteriogenesis or angiogenesis, was obtained in the form of increased matrix metalloproteinase-2 activity in them. These findings provide experimental evidence that chronic cerebral hypoperfusion would be protective against subsequent severe ischemic insults.

Original languageEnglish
Pages (from-to)89-97
Number of pages9
JournalCurrent Neurovascular Research
Volume4
Issue number2
DOIs
Publication statusPublished - 2007 May 1

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DNA-(Apurinic or Apyrimidinic Site) Lyase
Common Carotid Artery
Matrix Metalloproteinase 2
Oxidation-Reduction
Ligation
Wounds and Injuries
Infarction
Brain
Ischemia
Middle Cerebral Artery Infarction
Neurologic Manifestations
Reperfusion
Extracellular Matrix
Atherosclerosis
Pathologic Constriction
Arteries
Cell Count
Stroke
Staining and Labeling

All Science Journal Classification (ASJC) codes

  • Neurology
  • Developmental Neuroscience
  • Cellular and Molecular Neuroscience

Cite this

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title = "Preconditioning with chronic cerebral hypoperfusion reduces a focal cerebral ischemic injury and increases apurinic/apyrimidinic endonuclease/redox factor-1 and matrix metalloproteinase-2 expression",
abstract = "Atherosclerosis may cause severe stenosis of the arteries supplying the brain, which induces chronic cerebral hypoperfusion. Although an infarction often occurs in the chronically hypoperfused brain area, it has been uncertain whether the stroke severity is attenuated or increased when further decrease of blood flow occurs. To test the hypothesis that chronic cerebral hypoperfusion is protective against the subsequent severe ischemia, we examined the effect of chronic cerebral hypoperfusion on brains subjected to acute focal ischemia. Spontaneous hypertensive rats were subjected to middle cerebral artery occlusion/reperfusion four weeks after bilateral common carotid artery ligation (BCAL) or sham operation. The rats with BCAL had smaller infarctions, determined by 2,3,5-triphenyltetrazolium hydrochloride staining, and less severe neurologic deficits than those with sham operation. The number of DNAdamaged cells, examined by the in situ nick translation study, was significantly reduced in animals with BCAL. Immunoreactivity for apurinic/apyrimidinic endonuclease/redox factor-1, which plays a role in cellular defense mechanism, was markedly increased in those with BCAL. Indirect evidence of extracellular matrix remodeling, which might be associated with adaptive arteriogenesis or angiogenesis, was obtained in the form of increased matrix metalloproteinase-2 activity in them. These findings provide experimental evidence that chronic cerebral hypoperfusion would be protective against subsequent severe ischemic insults.",
author = "Choi, {Sun Ah} and Eum, {Hee Kim} and Jong, {Yun Lee} and Hyo, {Suck Nam} and Seo, {Hyun Kim} and Gyung, {Whan Kim} and Byung, {In Lee} and Jihoe Heo",
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Preconditioning with chronic cerebral hypoperfusion reduces a focal cerebral ischemic injury and increases apurinic/apyrimidinic endonuclease/redox factor-1 and matrix metalloproteinase-2 expression. / Choi, Sun Ah; Eum, Hee Kim; Jong, Yun Lee; Hyo, Suck Nam; Seo, Hyun Kim; Gyung, Whan Kim; Byung, In Lee; Heo, Jihoe.

In: Current Neurovascular Research, Vol. 4, No. 2, 01.05.2007, p. 89-97.

Research output: Contribution to journalArticle

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N2 - Atherosclerosis may cause severe stenosis of the arteries supplying the brain, which induces chronic cerebral hypoperfusion. Although an infarction often occurs in the chronically hypoperfused brain area, it has been uncertain whether the stroke severity is attenuated or increased when further decrease of blood flow occurs. To test the hypothesis that chronic cerebral hypoperfusion is protective against the subsequent severe ischemia, we examined the effect of chronic cerebral hypoperfusion on brains subjected to acute focal ischemia. Spontaneous hypertensive rats were subjected to middle cerebral artery occlusion/reperfusion four weeks after bilateral common carotid artery ligation (BCAL) or sham operation. The rats with BCAL had smaller infarctions, determined by 2,3,5-triphenyltetrazolium hydrochloride staining, and less severe neurologic deficits than those with sham operation. The number of DNAdamaged cells, examined by the in situ nick translation study, was significantly reduced in animals with BCAL. Immunoreactivity for apurinic/apyrimidinic endonuclease/redox factor-1, which plays a role in cellular defense mechanism, was markedly increased in those with BCAL. Indirect evidence of extracellular matrix remodeling, which might be associated with adaptive arteriogenesis or angiogenesis, was obtained in the form of increased matrix metalloproteinase-2 activity in them. These findings provide experimental evidence that chronic cerebral hypoperfusion would be protective against subsequent severe ischemic insults.

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