Temporal Profiles of Stress Protein Inductions after Focal Transient Ischemia in Mice Brain

Qian Li, Yumiko Nakano, Jingwei Shang, Yasuyuki Ohta, Kota Sato, Mami Takemoto, Nozomi Hishikawa, Toru Yamashita, Koji Abe

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Background Stress proteins have been found to play important protective roles against ischemic brain injury under hypoxic, oxidative, heat shock, and proteasome stresses. Methods In the present study, we investigated the temporal profiles of the major stress proteins including hypoxia-inducible factor-1α (HIF-1α), glutathione (GSH), heat shock protein 72 (HSP72), constitutive heat shock cognate protein 73 (HSC73), and ubiquitin after 45 minutes of transient middle cerebral artery occlusion (tMCAO) in the mice brain up to 7 days after reperfusion. Results Immunohistochemical analyses of HIF-1α, GSH, HSP72, and ubiquitin showed little immunoreactivity of neural cells in sham control brain, whereas HSC73 showed a constitutive immunoreactivity. After tMCAO, HSC73 showed the fastest increase at 12 hours in the peri-ischemic area, followed by HIF-1α with a peak at 24 hours, GSH, HSP72, and ubiquitin with a peak at 72 hours. All these stress proteins returned toward the baseline levels until 7 days. In the ischemic core, these stress proteins showed a similar change with less reaction compared to the peri-ischemic area. Conclusions These data showed temporal expressions of HIF-1α, GSH, HSP72, HSC73, and ubiquitin in the mice brain after tMCAO, which might provide a better understanding of neuroprotective mechanisms and novel targets for therapeutic intervention of brain ischemic disease.

Original languageEnglish
Pages (from-to)2344-2351
Number of pages8
JournalJournal of Stroke and Cerebrovascular Diseases
Volume25
Issue number10
DOIs
Publication statusPublished - Oct 1 2016

Fingerprint

Heat-Shock Proteins
Ischemia
HSP72 Heat-Shock Proteins
Hypoxia-Inducible Factor 1
Brain
Ubiquitin
Middle Cerebral Artery Infarction
Brain Diseases
Proteasome Endopeptidase Complex
Brain Injuries
Reperfusion
Glutathione
Shock
Hot Temperature

Keywords

  • Cerebral ischemia
  • GSH
  • HIF-1α
  • HSC73
  • HSP72
  • ubiquitin

ASJC Scopus subject areas

  • Surgery
  • Rehabilitation
  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine

Cite this

Temporal Profiles of Stress Protein Inductions after Focal Transient Ischemia in Mice Brain. / Li, Qian; Nakano, Yumiko; Shang, Jingwei; Ohta, Yasuyuki; Sato, Kota; Takemoto, Mami; Hishikawa, Nozomi; Yamashita, Toru; Abe, Koji.

In: Journal of Stroke and Cerebrovascular Diseases, Vol. 25, No. 10, 01.10.2016, p. 2344-2351.

Research output: Contribution to journalArticle

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AB - Background Stress proteins have been found to play important protective roles against ischemic brain injury under hypoxic, oxidative, heat shock, and proteasome stresses. Methods In the present study, we investigated the temporal profiles of the major stress proteins including hypoxia-inducible factor-1α (HIF-1α), glutathione (GSH), heat shock protein 72 (HSP72), constitutive heat shock cognate protein 73 (HSC73), and ubiquitin after 45 minutes of transient middle cerebral artery occlusion (tMCAO) in the mice brain up to 7 days after reperfusion. Results Immunohistochemical analyses of HIF-1α, GSH, HSP72, and ubiquitin showed little immunoreactivity of neural cells in sham control brain, whereas HSC73 showed a constitutive immunoreactivity. After tMCAO, HSC73 showed the fastest increase at 12 hours in the peri-ischemic area, followed by HIF-1α with a peak at 24 hours, GSH, HSP72, and ubiquitin with a peak at 72 hours. All these stress proteins returned toward the baseline levels until 7 days. In the ischemic core, these stress proteins showed a similar change with less reaction compared to the peri-ischemic area. Conclusions These data showed temporal expressions of HIF-1α, GSH, HSP72, HSC73, and ubiquitin in the mice brain after tMCAO, which might provide a better understanding of neuroprotective mechanisms and novel targets for therapeutic intervention of brain ischemic disease.

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