TY - JOUR
T1 - Enhanced phosphorylation of PTEN in rat brain after transient middle cerebral artery occlusion
AU - Omori, N.
AU - Jin, G.
AU - Li, F.
AU - Zhang, W. R.
AU - Wang, S. J.
AU - Hamakawa, Y.
AU - Nagano, I.
AU - Manabe, Y.
AU - Shoji, M.
AU - Abe, K.
N1 - Funding Information:
This work was partly supported by Grants-in-Aid for Scientific Research (B) 12470141, (Hoga) 12877211, and (Shorei) 13770377 from the Ministry of Education, Science, Culture and Sports of Japan, and by Grants (Tashiro K, Itoyama Y) and Comprehensive Research on Aging and Health (H11-Choju-010, No.207, Koizumi A) from the Ministry of Health and Welfare of Japan.
PY - 2002/11/8
Y1 - 2002/11/8
N2 - A phosphatase PTEN (phosphatase and tensin homologue deleted on chromosome 10) is a tumor suppressor gene that suppresses cell growth, inhibits cell migration, and induces apoptosis. Phosphorylated form of PTEN (p-PTEN) is a key survival factor relating PI3K-Akt pathway and their downstream effectors. A spatiotemporal profiles of PTEN and p-PTEN expression were immunohistochemically examined after 90 min of transient middle cerebral artery occlusion in rats. In the ischemic core, PTEN progressively decreased by 3 days, whereas a rapid but transient increase of p-PTEN was found with a peak at 1 h after the reperfusion. In contrast, in the ischemic penumbra, PTEN showed a minor change and a gradual but sustained p-PTEN expression was observed in the ischemic penumbra with a peak at 12 h. In addition, the balance of population among strongly, moderately, and weakly stained cells was different between the ischemic core and penumbra at their peak time points. These results suggest an important role of p-PTEN for cell survival after ischemia as an upstream regulator for PI3K-Akt.
AB - A phosphatase PTEN (phosphatase and tensin homologue deleted on chromosome 10) is a tumor suppressor gene that suppresses cell growth, inhibits cell migration, and induces apoptosis. Phosphorylated form of PTEN (p-PTEN) is a key survival factor relating PI3K-Akt pathway and their downstream effectors. A spatiotemporal profiles of PTEN and p-PTEN expression were immunohistochemically examined after 90 min of transient middle cerebral artery occlusion in rats. In the ischemic core, PTEN progressively decreased by 3 days, whereas a rapid but transient increase of p-PTEN was found with a peak at 1 h after the reperfusion. In contrast, in the ischemic penumbra, PTEN showed a minor change and a gradual but sustained p-PTEN expression was observed in the ischemic penumbra with a peak at 12 h. In addition, the balance of population among strongly, moderately, and weakly stained cells was different between the ischemic core and penumbra at their peak time points. These results suggest an important role of p-PTEN for cell survival after ischemia as an upstream regulator for PI3K-Akt.
KW - Akt
KW - Apoptosis
KW - MCAO
KW - PI3K
KW - PTEN
KW - Phospho-PTEN
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U2 - 10.1016/S0006-8993(02)03366-8
DO - 10.1016/S0006-8993(02)03366-8
M3 - Article
C2 - 12414116
AN - SCOPUS:0037044910
SN - 0006-8993
VL - 954
SP - 317
EP - 322
JO - Molecular Brain Research
JF - Molecular Brain Research
IS - 2
ER -