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IGF-I neuroprotection in the immature brain after hypoxia-ischemia, involvement of Akt and GSK3beta?

Artikel i vetenskaplig tidskrift
Författare Katarina Gustafsson Brywe
Carina Mallard
Malin Gustavsson
Maj Hedtjärn
Anna-Lena Leverin
Xiaoyang Wang
Klas Blomgren
Jörgen Isgaard
Henrik Hagberg
Publicerad i Eur J Neurosci
Volym 21
Nummer/häfte 6
Sidor 1489-502
ISSN 0953-816X (Print)
Publiceringsår 2005
Publicerad vid Institutionen för kvinnors och barns hälsa, Avdelningen för obstetrik och gynekologi
Institutionen för invärtesmedicin
Institutionen för kvinnors och barns hälsa, Avdelningen för pediatrik
Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi
Sidor 1489-502
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Animals, Animals, Newborn, Brain/drug effects/growth & development/metabolism, Glycogen Synthase Kinase 3/antagonists & inhibitors/genetics/*physiology, Humans, Hypoxia-Ischemia, Brain/genetics/metabolism/*prevention & control, Insulin-Like Growth Factor I/*physiology/*therapeutic use, Neuroprotective Agents/pharmacology/*therapeutic use, Protein-Serine-Threonine Kinases/biosynthesis/genetics/*physiology, Proto-Oncogene Proteins/biosynthesis/genetics/*physiology, Proto-Oncogene Proteins c-akt, Rats, Rats, Wistar
Ämneskategorier Experimentell hjärnforskning, Neurobiologi

Sammanfattning

Insulin-like growth factor I (IGF-I) is a neurotrophic factor that promotes neuronal growth, differentiation and survival. Neuroprotective effects of IGF-I have previously been shown in adult and juvenile rat models of brain injury. We wanted to investigate the neuroprotective effect of IGF-I after hypoxia-ischemia (HI) in 7-day-old neonatal rats and the mechanisms of IGF-I actions in vivo. We also wanted to study effects of HI and/or IGF-I on the serine/threonine kinases Akt and glycogen synthase kinase 3beta (GSK3beta) in the phophatidylinositol-3 kinase (PI3K) pathway. Immediately after HI, phosphorylated Akt (pAkt) and phosphorylated GSK3beta (pGSK3beta) immunoreactivity was lost in the ipsilateral and reduced in the contralateral hemisphere. After 45 min, pAkt levels were restored to control values, whereas pGSK3beta remained low 4 h after HI. Administration of IGF-I (50 microg i.c.v.) after HI resulted in a 40% reduction in brain damage (loss of microtubule-associated protein) compared with vehicle-treated animals. IGF-I treatment without HI was shown to increase pAkt whereas pGSK3beta decreased in the cytosol, but increased in the nuclear fraction. IGF-I treatment after HI increased pAkt in the cytosol and pGSK3beta in both the cytosol and the nuclear fraction in the ipsilateral hemisphere compared with vehicle-treated rats, concomitant with a reduced caspase-3- and caspase-9-like activity. In conclusion, IGF-I induces activation of Akt during recovery after HI which, in combination with inactivation of GSK3beta, may explain the attenuated activation of caspases and reduction of injury in the immature brain.

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