Affordable Access

CRE-mediated gene transcription in the peri-infarct area after focal cerebral ischemia in mice.

Authors
  • Sugiura, Shiro
  • Kitagawa, Kazuo
  • Omura-Matsuoka, Emi
  • Sasaki, Tsutomu
  • Tanaka, Shigeru
  • Yagita, Yoshiki
  • Matsushita, Kohji
  • Storm, Daniel R
  • Hori, Masatsugu
Type
Published Article
Journal
Journal of neuroscience research
Publication Date
Feb 01, 2004
Volume
75
Issue
3
Pages
401–407
Identifiers
PMID: 14743453
Source
Medline
License
Unknown

Abstract

Cyclic AMP response element binding protein (CREB) is a transcription factor expressed constitutively primarily in neurons and is activated by phosphorylation at Ser(133) residue. CREB mediates expression of several neuroprotective proteins, including B-cell CLL/lymphoma 2 (BCL-2) and brain-derived neurotrophic factor (BDNF). Although phosphorylation of CREB after ischemia has been investigated extensively, CRE-mediated gene transcription after ischemia is not as well studied. We investigated temporal changes in CRE-mediated gene transcription in the cerebral cortex after focal ischemia in transgenic mice with a CRE-lacZ reporter gene. In the ischemic core, X-gal-positive cells, which reflected expression of the CRE-lacZ reporter gene, were observed rarely at any time point, though transient phosphorylation of CREB was detected. In contrast, the peri-infarct area showed a persistent increase in the number of X-gal-positive cells, of which more than half were positive for neuronal nuclei (NeuN). Our results suggest that CRE-mediated gene transcription, the pattern of which is not always consistent with that of CREB phosphorylation, occurs primarily in neurons in the peri-infarct area after focal cerebral ischemia and may be a neuroprotective response against ischemic insult.

Report this publication

Statistics

Seen <100 times