|  Help  |  About  |  Contact Us

Publication : Hyperthermic preconditioning protects astrocytes from ischemia/reperfusion injury by up-regulation of HIF-1 alpha expression and binding activity.

First Author  Du F Year  2010
Journal  Biochim Biophys Acta Volume  1802
Issue  11 Pages  1048-53
PubMed ID  20599612 Mgi Jnum  J:170024
Mgi Id  MGI:4943811 Doi  10.1016/j.bbadis.2010.06.013
Citation  Du F, et al. (2010) Hyperthermic preconditioning protects astrocytes from ischemia/reperfusion injury by up-regulation of HIF-1 alpha expression and binding activity. Biochim Biophys Acta 1802(11):1048-53
abstractText  It has been demonstrated that hypoxia-inducible factor-1 alpha (HIF-1 alpha) mediates ischemic tolerance induced by hypoxia/ischemia or pharmacological preconditioning. In addition, preconditioning stimuli can be cross-tolerant, safeguarding against other types of injury. We therefore hypothesized HIF-1 alpha might also be associated with ischemic tolerance induced by hyperthermic preconditioning. In the present study, we demonstrated for the first time that 6 h of hyperthermia (38 degrees C or 40 degrees C) could induce a characteristic 'reactive' morphology and a significant increase in the expression of bystin in astrocytes. We also showed that pre-treatment with 6 h of hyperthermia resulted in a significant increase in cell viability and a remarkable decrease in lactate dehydrogenase (LDH) release and apoptosis development in the astrocytes that were exposed to 24 h of ischemia and a subsequent 24 h of reperfusion. Analysis of mechanisms showed that hyperthermia could lead to a significant increase in HIF-1 alpha expression and also the HIF-1 binding activity in the ischemia/reperfusion astrocytes. The data provide evidence to our hypothesis that the up-regulation of HIF-1 alpha is associated with the protective effects of hyperthermic preconditioning on astrocytes against ischemia/reperfusion injury.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

6 Authors

1 Bio Entities

0 Expression