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Oestrogen Prevention of Neural Cell Death Correlates with Decreased Expression of mRNA for the Pro‐Apoptotic Protein Nip‐2
Author(s) -
Meda C.,
Vegeto E.,
Pollio G.,
Ciana P.,
Patrone C.,
Pellicciari C.,
Maggi A.
Publication year - 2000
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 - 10.1046/j.1365-2826.2000.00541.x
Subject(s) - nip , apoptosis , programmed cell death , messenger rna , endocrinology , medicine , neuroblastoma , biology , antagonist , receptor , dna fragmentation , cell , cell culture , microbiology and biotechnology , cancer research , gene , biochemistry , genetics , computer science , programming language
We have recently identified nip‐2 as a gene target for 17β‐oestradiol activity in the neuroblastoma SK‐ER 3 cells expressing the oestrogen receptor (ER) α. Here we show 17β‐oestradiol treatment of neuroblastoma and rat embryo neurones in culture blocks the increase in nip‐2 mRNA induced by apoptotic stimuli and prevents cell death as indicated by cell counting, 3,(4,5‐dimethylthiazol‐2‐yl)2,5‐diphenil‐tetrazoliumbromide and DNA fragmentation assays. Neither of these effects are observed in the presence of the specific ER antagonist ICI 182,780, and are absent in neuroblastoma cells not expressing ER. We propose that nip‐2 plays a relevant role in neural cell apoptosis and that a decrease in its expression is instrumental for the oestrogen anti‐apoptotic effect described here. The experimental evidence presented supports the recent hypothesis of a protective role of oestrogens in neurodegenerative diseases such as Alzheimer's disease and highlights the importance of the development of new ER ligands for the prevention of neural cell damage.