Involvement of MAPK/ERK kinase-ERK pathway in exogenous bFGF-induced Egr-1 binding activity enhancement in anoxia-reoxygenation injured astrocytes.
- Author:
Ying LIU
1
;
Jin-Biao LU
;
Qi CHEN
;
Zhu-Rong YE
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Animals, Newborn; Astrocytes; drug effects; metabolism; Cells, Cultured; Early Growth Response Protein 1; metabolism; Electrophoretic Mobility Shift Assay; methods; Fibroblast Growth Factors; pharmacology; Mitogen-Activated Protein Kinase Kinases; metabolism; Oxygen; metabolism; Protein Binding; drug effects; Rats; Signal Transduction; physiology; Time Factors
- From: Neuroscience Bulletin 2007;23(4):221-228
- CountryChina
- Language:English
-
Abstract:
OBJECTIVEIntravenous administration of basic fibroblast growth factor (bFGF) is effective to reduce the volume of cerebral infract due to ischemia. This study was designed to investigate the molecular mechanism, especially the signal transduction pathways, involved in this protective role of bFGF.
METHODSAnoxia-reoxygenation treated astrocytes were used to study the role of mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (MAPK/ERK kinase, MEK)-ERK signaling pathway after exogenous bFGF administration by Western blot. Electrophoretic mobile shift assay was used to detect the binding activity of early growth response factor-1 (Egr-1), an important transcription factor for endogenous bFGF.
RESULTSbFGF could protect some signal transduction proteins from the oxygen-derived free radicals induced degradation. ERK1/2 was activated and involved in Egr-1 binding activity enhancement induced by exogenous bFGF.
CONCLUSIONMEK-ERK MAPK cascade may be an important signal transduction pathway contributed to bFGF induced enhancement of Egr-1 binding activity in anoxia-reoxygenation injured astrocytes.
