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Retinoic acid‐ and phorbol ester‐induced neuronal differentiation down‐regulates caveolin expression in GnRH neurons
Author(s) -
D’Orlando Cristina,
Guzzi Francesca,
Gravati Marta,
Biella Gerardo,
Toselli Mauro,
Meneveri Raffaella,
Barisani Donatella,
Parenti Marco
Publication year - 2008
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2007.05109.x
Subject(s) - retinoic acid , microbiology and biotechnology , estrogen receptor beta , cellular differentiation , biology , estrogen receptor , caveolae , medicine , caveolin , estrogen receptor alpha , p19 cell , endocrinology , cell culture , chemistry , signal transduction , biochemistry , genetics , cancer , adult stem cell , breast cancer , gene
J. Neurochem . (2008) 104, 1577–1587. Abstract GN11 and GT1‐7 are immortalized gonadotropin‐releasing hormone‐positive murine cell lines exhibiting the features of immature olfactory neurons and differentiated hypothalamic neurons, respectively. Using electron microscopy and biochemical assays (RT‐PCR and immunoblotting) we determined the presence of numerous caveolae invaginations and of caveolin‐1 and ‐2 mRNAs and proteins in GN11 cells, and their absence in GT1‐7 cells. The lack of caveolins in GT1‐7 cells might be due to the silencing of gene transcription caused by estrogen receptor α whose inhibitory activity in GN11 cells could be counter‐balanced by co‐expression of caveolin‐permissive estrogen receptor β. To test whether the unique expression of caveolins in GN11 cells is related to their immature state, we treated GN11 cells for 24–72 h with retinoic acid or phorbol ester. Both treatments led to neuronal differentiation of GN11 cells, as shown by emission of long neuritic processes, increased expression of growth cone‐associated protein‐43 and appearance of voltage‐gated K + and Ca 2+ channel currents. Concurrently, caveolins 1 and 2, and estrogen receptor β were down‐regulated in differentiated GN11, whereas estrogen receptor α was unaffected by differentiation. We conclude that caveolin expression in GN11 neurons is down‐regulated upon differentiation and up‐regulated by estrogen receptor β.