IGF-I protects cortical neurons against ceramide-induced apoptosis via activation of the PI-3K/Akt and ERK pathways; is this protection independent of CREB and Bcl-2 ?
type: Dataset
description: Current understanding of IGF-I-mediated neuroprotection implies the activation of phosphatidylinositol-3-kinase (PI-3K), which leads to the activation of Akt/Protein Kinase B. In non-neuronal cells, Akt phosphorylates and activates the transcription factor CREB, implicated in the transcription of the anti-apoptotic bcl-2 gene. This paper further analyses the anti-apoptotic IGF-I action in neurons. We show that IGF-I protects cortical neurons against ceramide-induced apoptosis. Ceramide decreases Akt phosphorylation during apoptotic process whereas a simultaneous treatment with IGF-I increases Akt phosphorylation. Analysis of the signal transduction pathways revealed that IGF-I induces CREB phosphorylation via PI-3K and ERK, whereas simultaneous ceramide and IGF-I treatment decreases CREB phosphorylation. Although an overexpression of Bcl-2 protects cortical neurons against ceramide-induced apoptosis, our data indicate that the Bcl-2 protein level is not modulated during IGF-I, ceramide and/or LY294002 treatment. In consequence, we demonstrated that IGF protects neurons against ceramide-induced apoptosis and that IGF-I protection involves the PI-3K/Akt and ERK pathways; this protection may be independent of CREB and Bcl-2.
landing page: 0169-328X
keyword: cortex
keyword: infoeu-reposemanticsarticle
keyword: journal-articles
keyword: primary-culture
keyword: sdvneusclife-sciences-q-bioneurons-and-cognition-q-bionccognitive-sciences
keyword: signal-transduction
issued: 2026-05-11T03:07:30.946953
modified: 2026-05-11T03:07:30.946957
language: en
contact point: Organization
  fn: CCSD

test_moissonnage_selune
type: Agent

IGF-I protects cortical neurons against ceramide-induced apoptosis via activation of the PI-3K/Akt and ERK pathways; is this protection independent of CREB and Bcl-2 ?
type: Distribution
format: HTML
access URL: https://hal.science/hal-00082315
issued: 2026-05-11T03:07:30.954435
modified: 2026-05-11T03:07:30.937788