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Differentiation of mesencephalic neural cells changes estrogen-dependent ERK1/2 kinetic by means of caveolin-1

¹ Dipart. di Scienze della Vita, II Università di Napoli, Caserta, Italy,
² IGB-"ABT", Consiglio Nazionale delle Ricerche, Napoli, Italy,
³ Dipart. Scienze della Salute, Università del Molise, Campobasso, Italy,
⁴ Dipart. di Patologia generale, II Università di Napoli, Napoli, Italy

ABSTRACT

Estrogens influence a plethora of cellular functions including proliferation, differentiation, survival and neurotransmission, thus raising the question of the molecular mechanisms underlying these effects. We aimed at studying the biological effects of estrogens, according to the differentiation and proliferation status of neural cells. Here, we report that mesencephalic embryonic cells, either mes-c-myc A1 cell line or primary cultures, expressed estrogen receptor a (ERa) and that stimulation of 17b-estradiol (E2) lead to ERK1/2 activation. Following the arrest of proliferation and the onset of differentiation, we observed a change in the kinetic of ERK1/2 phosphorylation induced by E2 stimulation. Moreover, we showed that caveolin-1, a main constituent of caveolae in the plasma membrane lipidic rafts, was endogenously expressed, co-localizes with ERa on plasma membrane and was consistently up-regulated following differentiation and cell growth arrest. Treatment of proliferating and non-proliferating cells with â-cyclodextrin, a drug interfering with caveolae, equalized ERKs phosphorylation in response to E2 stimulation. In conclusion, we showed that ERK phosphorylation in response to E2 is dependent on differentiation and/or proliferation status and involved caveolin-1 and caveolae

This Article Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Colucci-D’Amato, L. Articles by Volpicelli, F. PubMed Articles by Colucci-D’Amato, L. Articles by Volpicelli, F.