Astrocytes Regulate the Expression of Insulin-Like Growth Factor 1 Receptor (IGF1-R) in Primary Cortical Neurons During In Vitro Senescence

The role of insulin-like growth factor 1 (IGF1) pathway as regulator of aging and age-related diseases is increasingly recognized. Recent evidence has been provided that neuronal IGF1-R increases during aging leading to activation of a signaling pathway that causes an increased production of amyloid...

Full description

Saved in:
Bibliographic Details
Published in:Journal of molecular neuroscience 2010-03, Vol.40 (3), p.342-352
Main Authors: Costantini, Claudio, Lorenzetto, Erika, Cellini, Barbara, Buffelli, Mario, Rossi, Filippo, Della-Bianca, Vittorina
Format: Article
Language:English
Subjects:
Age
Aging
Aging - physiology
Alzheimer's disease
Animals
Astrocytes
Astrocytes - cytology
Astrocytes - metabolism
beta -Amyloid
Biomedical and Life Sciences
Biomedicine
Cell Biology
Cell culture
Cells, Cultured
Cerebral Cortex - cytology
Cerebral Cortex - physiology
Coculture Techniques
Cortex
Culture Media, Conditioned - metabolism
Disease
Insulin
Insulin-like growth factor I
Insulin-like growth factors
Laboratory animals
Molecular weight
Nervous system
Neurochemistry
Neurodegenerative diseases
Neurology
Neurons
Neurons - cytology
Neurons - metabolism
Neurosciences
Pathology
Penicillin
Proteomics
Rats
Rats, Sprague-Dawley
Receptor, IGF Type 1 - metabolism
Senescence
Signal transduction
Signal Transduction - physiology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The role of insulin-like growth factor 1 (IGF1) pathway as regulator of aging and age-related diseases is increasingly recognized. Recent evidence has been provided that neuronal IGF1-R increases during aging leading to activation of a signaling pathway that causes an increased production of amyloid β-peptide, the principal event in the pathogenesis of Alzheimer’s disease. Here, by using long-term neuronal cultures as a model of aging, we show that astroglial cells are required to upregulate the expression of IGF1-R in neurons during in vitro senescence. Moreover, evidence is provided that the cross-talk between astrocytes and neurons is independent of cell-to-cell contact, and it is mediated by low molecular weight soluble factor(s) released by astrocytes in culture medium. These results suggest that astrocytes could play an important role in aging and age-related pathological processes.
ISSN:0895-8696
1559-1166
DOI:10.1007/s12031-009-9305-5