Relationship Between the Neuroprotective Effects of Insulin-Like Growth Factor-1 and 17[beta]-Oestradiol in Human Neuroblasts

Insulin-like growth factor-1 (IGF-1) and oestrogens interact with each other as neuroprotective factors. We have previously demonstrated that 17[beta]-oestradiol protects against [beta]-amyloid and oxidative stress toxicity and increases the amount of cell cholesterol in human foetal neuroblasts (FN...

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Published in:Journal of neuroendocrinology Vol. 24; no. 10; p. 1304
Main Authors: Luciani, P, Deledda, C, Benvenuti, S, Cellai, I, Modi, G, Fibbi, B, Danza, G, Vannelli, G B, Peri, A
Format: Journal Article
Language:English
Published: Oxford Wiley Subscription Services, Inc 01-10-2012
Online Access:Get full text
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Summary:Insulin-like growth factor-1 (IGF-1) and oestrogens interact with each other as neuroprotective factors. We have previously demonstrated that 17[beta]-oestradiol protects against [beta]-amyloid and oxidative stress toxicity and increases the amount of cell cholesterol in human foetal neuroblasts (FNC). The present study aimed: (i) to assess the protective effects of IGF-1 in FNC cells; (ii) to investigate the relationship between IGF-1 and 17[beta]-oestradiol; and (iii) to determine whether cholesterol was a major mediator of the effects of IGF-1, similarly to 17[beta]-oestradiol. We found that IGF-1 effectively exerts neuroprotective effects in FNC cells. We also demonstrated that the IGF-1 receptor (IGF-1R) pathway is needed to maintain oestrogen-mediated neuroprotection. Finally, we found that, opposite to 17[beta]-oestradiol, IGF-1 did not cause a significant increase in cell cholesterol. These findings indicate that a cross-talk between IGF-1 and 17[beta]-oestradiol occurs in FNC cells. In particular, the activation of the IGF-1R cascade appears to be fundamental to warrant 17[beta]-oestradiol-mediated neuroprotection, even though cell cholesterol does not play a major role as an effector of this pathway. [PUBLICATION ABSTRACT]
ISSN:0953-8194
1365-2826
DOI:10.1111/j.1365-2826.2012.02343.x