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Estradiol Modulates Insulin‐Like Growth Factor I Receptors and Binding Proteins in Neurons from the Hypothalamus
Author(s) -
Pons S.,
TorresAleman I.
Publication year - 1993
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.1365-2826.1993.tb00482.x
Subject(s) - endocrinology , medicine , hypothalamus , receptor , insulin like growth factor , insulin , biology , chemistry , growth factor
Trophic effects of 17β‐estradiol (βE 2 ) on in vitro developing hypothalamic cells have been reported. Insulin‐like growth factor I (IGF‐I) is also a potent trophic factor for cultured hypothalamic cells. An interaction between sexual steroids and insulin‐like growth factors (IGFs) in modulating growth of hypothalamic cells has been suggested. Thus, we tested whether βE 2 modulates the levels of IGF‐I, its membrane receptor and its binding proteins in rat hypothalamic culturs. Using both neuron‐ and glial‐enriched cultures obtained from fetal rat hypothalami we found that addition of βE 2 elicited a significant increase in IGF‐I receptor levels in neurons, without affecting its affinity. On the other hand, the three different IGF‐binding proteins (IGFBPs) found in the conditioned medium of the cultures were differentially modulated by βE 2 in the two types of cells studied. Overall, neuronal cultures produced greater amounts of IGFBPs after treatment with βE 2 , with IGFBP2 reaching significantly higher levels. On the contrary, treatment with βE 2 did not significantly alter the amounts of IGFBPs produced by glial cells. Finally, the levels of immunoreactive IGF‐I found either in the medium or in cellular extracts in both neuronal and glial cultures were not modified by treatment with βE 2 . These results strongly support previous observations of a trophic synergistic interaction between IGFs and βE 2 on hypothalamic cells. Thus, an increase in IGF‐I receptors and/or IGFBPs after exposure to βE 2 may result in an enhanced response of hypothalamic neurons to IGF‐I. Further, the present findings strengthen our recent observation that the effects of βE 2 on hypothalamic glial cells are neuronally mediated, since IGF‐I receptors and IGFBPs are modulated by this sex hormone in neurons, but not in glial cells.