Abstract:
BACKGROUND AND PURPOSE:The integrin-linked kinase (ILK) signaling pathway contributes to regulation of cellular adhesion, migration, and differentiation, and to apoptotic cell death after a variety of cell death stimuli. We have reported that overexpression of copper/zinc superoxide dismutase (SOD1) reduces apoptotic cell death by promoting the phosphatidylinositol 3-kinase (PI3-K)/Akt survival pathway after transient focal cerebral ischemia (tFCI). However, the role of the ILK pathway after tFCI and the role of oxygen free radicals in regulation of apoptosis remain unclear. METHODS:To clarify these issues, we used an in vivo tFCI model with SOD1 transgenic mice and wild-type mice. We administered the PI3-K inhibitor, LY294002, into mouse brains after tFCI and examined the role of PI3-K in the ILK pathway and expression of the ILK/Akt complex by immunohistochemistry, Western blot analysis, and coimmunoprecipitation. RESULTS:A transient increase in ILK was detected early after tFCI and was prevented by treatment with LY294002, but promoted by SOD1. Coimmunoprecipitation revealed that the direct reaction of ILK/Akt transiently increased concurrent with the increase in ILK after tFCI. Moreover, the ILK/Akt complex was prevented by LY294002, but promoted by SOD1. CONCLUSIONS:These results suggest that the ILK pathway mediated by PI3-K is affected by tFCI and by SOD1.
journal_name
Strokejournal_title
Strokeauthors
Saito A,Hayashi T,Okuno S,Nishi T,Chan PHdoi
10.1161/01.STR.0000144653.32853.edsubject
Has Abstractpub_date
2004-11-01 00:00:00pages
2560-5issue
11eissn
0039-2499issn
1524-4628pii
01.STR.0000144653.32853.edjournal_volume
35pub_type
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