Abstract:
:We studied whether pro-survival Akt was activated after transient focal cerebral ischemia and whether it inhibited pro-apoptotic Bad. Phosphorylation of Akt (serine-473) was enhanced in cortex after 1-hour ischemia, and also after 1h and 6 h of reperfusion, but it returned back to that in controls by 24 h. After this first wave of Akt activation, a second increase was observed between 4 and 7 days. In striatum, only the late Akt activation was seen. In contrast to Akt, no Bad phosphorylation (serine-136) was detected after ischemia. Therefore, injury spontaneously activated Akt, but this did not suppress Bad signalling. It is proposed that further pharmacological activation of Akt shortly after ischemia might promote cell survival, whereas Akt activation at longer time points is involved with glial reactivity.
journal_name
Neuroreportjournal_title
Neuroreportauthors
Friguls B,Justicia C,Pallàs M,Planas AMdoi
10.1097/00001756-200110290-00046subject
Has Abstractpub_date
2001-10-29 00:00:00pages
3381-4issue
15eissn
0959-4965issn
1473-558Xjournal_volume
12pub_type
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