Protection against ischemic brain damage by GDNF affecting cell survival and death signals

G. Jin; N. Omori; F. Li; I. Nagano; Y. Manabe; M. Shoji; K. Abe

doi:10.1179/016164103101201454

Protection against ischemic brain damage by GDNF affecting cell survival and death signals

G. Jin, N. Omori, F. Li, I. Nagano, Y. Manabe, M. Shoji, K. Abe

Research output: Contribution to journal › Article › peer-review

50 Citations (Scopus)

Abstract

Neuroprotective effects of glial cell line-derived neurotrophic factor (GDNF) on cell survival and death signals were investigated after 90min of transient middle cerebral artery occlusion (MCAO) in rats. Immunoreactivities of phosphorylated Akt (p-Akt), cleaved caspase-9 (c-cas9), and -3 (c-cas3) increased after the reperfusion in the penumbra in vehicle group with peaks at 3 h, 8 h, and 1 day, respectively. Topical application of GDNF (6.8 μg/9 μl) on brain surface potentiated and prolonged-Akt activation, but suppressed activation of the caspases, and reduced the number of terminal deoxynucleotidyl transferasemediated dUDP-biotin in situ nick labeling (TUNEL) positive cells. These results suggest that GDNF plays a protective role against ischemic injury by controlling the balance between Akt pathway and caspase cascades.

Original language	English
Pages (from-to)	249-253
Number of pages	5
Journal	Neurological Research
Volume	25
Issue number	3
DOIs	https://doi.org/10.1179/016164103101201454
Publication status	Published - Apr 1 2003

Keywords

Akt
Caspase-3
Caspase-9
Glial cell line-derived neurotrophic factor (GDNF)
Ischemia
Rat

ASJC Scopus subject areas

Neurology
Clinical Neurology

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title = "Protection against ischemic brain damage by GDNF affecting cell survival and death signals",

abstract = "Neuroprotective effects of glial cell line-derived neurotrophic factor (GDNF) on cell survival and death signals were investigated after 90min of transient middle cerebral artery occlusion (MCAO) in rats. Immunoreactivities of phosphorylated Akt (p-Akt), cleaved caspase-9 (c-cas9), and -3 (c-cas3) increased after the reperfusion in the penumbra in vehicle group with peaks at 3 h, 8 h, and 1 day, respectively. Topical application of GDNF (6.8 μg/9 μl) on brain surface potentiated and prolonged-Akt activation, but suppressed activation of the caspases, and reduced the number of terminal deoxynucleotidyl transferasemediated dUDP-biotin in situ nick labeling (TUNEL) positive cells. These results suggest that GDNF plays a protective role against ischemic injury by controlling the balance between Akt pathway and caspase cascades.",

keywords = "Akt, Caspase-3, Caspase-9, Glial cell line-derived neurotrophic factor (GDNF), Ischemia, Rat",

author = "G. Jin and N. Omori and F. Li and I. Nagano and Y. Manabe and M. Shoji and K. Abe",

note = "Funding Information: This work was partly supported by Grants-in-Aid for Scientific Research (B) 12470141 and (Hoga) 12877211 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.",

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doi = "10.1179/016164103101201454",

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pages = "249--253",

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T1 - Protection against ischemic brain damage by GDNF affecting cell survival and death signals

AU - Jin, G.

AU - Omori, N.

AU - Li, F.

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 and (Hoga) 12877211 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 - 2003/4/1

Y1 - 2003/4/1

N2 - Neuroprotective effects of glial cell line-derived neurotrophic factor (GDNF) on cell survival and death signals were investigated after 90min of transient middle cerebral artery occlusion (MCAO) in rats. Immunoreactivities of phosphorylated Akt (p-Akt), cleaved caspase-9 (c-cas9), and -3 (c-cas3) increased after the reperfusion in the penumbra in vehicle group with peaks at 3 h, 8 h, and 1 day, respectively. Topical application of GDNF (6.8 μg/9 μl) on brain surface potentiated and prolonged-Akt activation, but suppressed activation of the caspases, and reduced the number of terminal deoxynucleotidyl transferasemediated dUDP-biotin in situ nick labeling (TUNEL) positive cells. These results suggest that GDNF plays a protective role against ischemic injury by controlling the balance between Akt pathway and caspase cascades.

AB - Neuroprotective effects of glial cell line-derived neurotrophic factor (GDNF) on cell survival and death signals were investigated after 90min of transient middle cerebral artery occlusion (MCAO) in rats. Immunoreactivities of phosphorylated Akt (p-Akt), cleaved caspase-9 (c-cas9), and -3 (c-cas3) increased after the reperfusion in the penumbra in vehicle group with peaks at 3 h, 8 h, and 1 day, respectively. Topical application of GDNF (6.8 μg/9 μl) on brain surface potentiated and prolonged-Akt activation, but suppressed activation of the caspases, and reduced the number of terminal deoxynucleotidyl transferasemediated dUDP-biotin in situ nick labeling (TUNEL) positive cells. These results suggest that GDNF plays a protective role against ischemic injury by controlling the balance between Akt pathway and caspase cascades.

KW - Akt

KW - Caspase-3

KW - Caspase-9

KW - Glial cell line-derived neurotrophic factor (GDNF)

KW - Ischemia

KW - Rat

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Protection against ischemic brain damage by GDNF affecting cell survival and death signals

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