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Caveolin-1 is involved in reactive oxygen species-induced SHP-2 activation in astrocytes

Title
Caveolin-1 is involved in reactive oxygen species-induced SHP-2 activation in astrocytes
Authors
Yun J.H.Park S.J.Jo A.Kang J.L.Jou I.Park J.S.Choi Y.-H.
Ewha Authors
이지희최윤희
SCOPUS Author ID
이지희scopus; 최윤희scopus
Issue Date
2011
Journal Title
Experimental and Molecular Medicine
ISSN
1226-3613JCR Link
Citation
vol. 43, no. 12, pp. 660 - 668
Indexed
SCI; SCIE; SCOPUS; KCI WOS scopus
Abstract
Recent evidence supports a neuroprotective role of Src homology 2-containing protein tyrosine phosphatase 2 (SHP-2) against ischemic brain injury. However, the molecular mechanisms of SHP-2 activation and those governing how SHP-2 exerts its function under oxidative stress conditions are not well understood. Recently we have reported that reactive oxygen species (ROS)-mediated oxidative stress promotes the phosphorylation of endogenous SHP-2 through lipid rafts, and that this phosphorylation strongly occurs in astrocytes, but not in microglia. To investigate the molecules involved in events leading to phosphorylation of SHP-2, raft proteins were analyzed using astrocytes and microglia. Interestingly, caveolin-1 and -2 were detected only in astrocytes but not in microglia, whereas flotillin-1 was expressed in both cell types. To examine whether the H 2O 2-dependent phosphorylation of SHP-2 is mediated by caveolin-1, we used specific small interfering RNA (siRNA) to downregulate caveolin- 1 expression. In the presence of caveolin-1 siRNA, the level of SHP-2 phosphorylation induced by H 2O 2 was significantly decreased, compared with in the presence of control siRNA. Overexpression of caveolin- 1 effectively increased H 2O 2-induced SHP-2 phosphorylation in microglia. Lastly, H 2O 2 induced extracellular signal-regulated kinase (ERK) activation in astrocytes through caveolin-1. Our results suggest that caveolin-1 is involved in astrocyte-specific intracellular responses linked to the SHP-2-mediated signaling cascade following ROS-induced oxidative stress.
DOI
10.3858/emm.2011.43.12.075
Appears in Collections:
의과대학 > 의학과 > Journal papers
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