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Relationship Between the Neuroprotective Effects of Insulin‐Like Growth Factor‐1 and 17β‐Oestradiol in Human Neuroblasts
Author(s) -
Luciani P.,
Deledda C.,
Benvenuti S.,
Cellai I.,
Modi G.,
Fibbi B.,
Danza G.,
Vannelli G. B.,
Peri A.
Publication year - 2012
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.2012.02343.x
Subject(s) - neuroprotection , neuroblast , endocrinology , medicine , insulin like growth factor , growth factor , mediator , oxidative stress , biology , chemistry , receptor , microbiology and biotechnology , neurogenesis
Insulin‐like growth factor‐1 (IGF‐1) and oestrogens interact with each other as neuroprotective factors. We have previously demonstrated that 17β‐oestradiol protects against β‐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 17β‐oestradiol; and (iii) to determine whether cholesterol was a major mediator of the effects of IGF‐1, similarly to 17β‐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 17β‐oestradiol, IGF‐1 did not cause a significant increase in cell cholesterol. These findings indicate that a cross‐talk between IGF‐1 and 17β‐oestradiol occurs in FNC cells. In particular, the activation of the IGF‐1R cascade appears to be fundamental to warrant 17β‐oestradiol‐mediated neuroprotection, even though cell cholesterol does not play a major role as an effector of this pathway.