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Title: Enhanced phosphorylation of cyclic AMP response element binding protein in Brain of mice following repetitive hypoxic exposure

Abstract

Cerebral ischemic/hypoxic preconditioning (I/HPC) is a phenomenon of endogenous protection that renders Brain tolerant to sustained ischemia/hypoxia. This profound protection induced by I/HPC makes it an attractive target for developing potential clinical therapeutic approaches. However, the molecular mechanism of I/HPC is unclear. Cyclic AMP (cAMP) response element binding protein (CREB), a selective nuclear transcriptional factor, plays a key role in the neuronal functions. Phosphorylation of CREB on Ser-133 may facilitate its transcriptional activity in response to various stresses. In the current study, we observed the changes in CREB phosphorylation (Ser-133) and protein expression in Brain of auto-hypoxia-induced HPC mice by using Western blot analysis. We found that the levels of phosphorylated CREB (Ser-133), but not protein expression of CREB, increased significantly (p < 0.05) in the hippocampus and the frontal cortex of mice after repetitive hypoxic exposure (H2-H4, n = 6 for each group), when compared to that of the normoxic (H0, n = 6) or hypoxic exposure once group (H1, n = 6). In addition, a significant enhancement (p < 0.05) of CREB phosphorylation (Ser-133) could also be found in the nuclear extracts from the whole hippocampus of hypoxic preconditioned mice (H2-H4, n = 6 for each group). Thesemore » results suggest that the phosphorylation of CREB might be involved in the development of cerebral hypoxic preconditioning.« less

Authors:
 [1];  [1];  [1];  [1];  [1];  [2];  [3]
  1. Institute for Biomedical Science of Pain, Beijing Key Laboratory for Neural Regeneration and Repairing, Department of Neurobiology, Capital University of Medical Sciences, No. 10 You AnMen Wai Xi Tou Tiao, Beijing 100054 (China)
  2. Division of Neurosurgery, Department of Surgery, Neuroscience and Cell Biology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-0517 (United States). E-mail: lfang@utmb.edu
  3. Institute for Biomedical Science of Pain, Beijing Key Laboratory for Neural Regeneration and Repairing, Department of Neurobiology, Capital University of Medical Sciences, No. 10 You AnMen Wai Xi Tou Tiao, Beijing 100054 (China). E-mail: junfali@cpums.edu.cn
Publication Date:
OSTI Identifier:
20798798
Resource Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 340; Journal Issue: 2; Other Information: DOI: 10.1016/j.bbrc.2005.12.064; PII: S0006-291X(05)02818-4; Copyright (c) 2005 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; AMP; ANOXIA; BIOLOGICAL STRESS; HIPPOCAMPUS; ISCHEMIA; MICE; PHOSPHORYLATION; PROTEINS

Citation Formats

Gao Yanan, Gao Ge, Long Caixia, Han Song, Zu Pengyu, Fang Li, and Li Junfa. Enhanced phosphorylation of cyclic AMP response element binding protein in Brain of mice following repetitive hypoxic exposure. United States: N. p., 2006. Web.
Gao Yanan, Gao Ge, Long Caixia, Han Song, Zu Pengyu, Fang Li, & Li Junfa. Enhanced phosphorylation of cyclic AMP response element binding protein in Brain of mice following repetitive hypoxic exposure. United States.
Gao Yanan, Gao Ge, Long Caixia, Han Song, Zu Pengyu, Fang Li, and Li Junfa. Fri . "Enhanced phosphorylation of cyclic AMP response element binding protein in Brain of mice following repetitive hypoxic exposure". United States. doi:.
@article{osti_20798798,
title = {Enhanced phosphorylation of cyclic AMP response element binding protein in Brain of mice following repetitive hypoxic exposure},
author = {Gao Yanan and Gao Ge and Long Caixia and Han Song and Zu Pengyu and Fang Li and Li Junfa},
abstractNote = {Cerebral ischemic/hypoxic preconditioning (I/HPC) is a phenomenon of endogenous protection that renders Brain tolerant to sustained ischemia/hypoxia. This profound protection induced by I/HPC makes it an attractive target for developing potential clinical therapeutic approaches. However, the molecular mechanism of I/HPC is unclear. Cyclic AMP (cAMP) response element binding protein (CREB), a selective nuclear transcriptional factor, plays a key role in the neuronal functions. Phosphorylation of CREB on Ser-133 may facilitate its transcriptional activity in response to various stresses. In the current study, we observed the changes in CREB phosphorylation (Ser-133) and protein expression in Brain of auto-hypoxia-induced HPC mice by using Western blot analysis. We found that the levels of phosphorylated CREB (Ser-133), but not protein expression of CREB, increased significantly (p < 0.05) in the hippocampus and the frontal cortex of mice after repetitive hypoxic exposure (H2-H4, n = 6 for each group), when compared to that of the normoxic (H0, n = 6) or hypoxic exposure once group (H1, n = 6). In addition, a significant enhancement (p < 0.05) of CREB phosphorylation (Ser-133) could also be found in the nuclear extracts from the whole hippocampus of hypoxic preconditioned mice (H2-H4, n = 6 for each group). These results suggest that the phosphorylation of CREB might be involved in the development of cerebral hypoxic preconditioning.},
doi = {},
journal = {Biochemical and Biophysical Research Communications},
number = 2,
volume = 340,
place = {United States},
year = {Fri Feb 10 00:00:00 EST 2006},
month = {Fri Feb 10 00:00:00 EST 2006}
}
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