17β-estradiol (E2) plays a crucial role in the maintenance of body homeostasis including the balance
between cell survival and apoptosis. Intriguingly, estrogen receptor subtypes (i.e., ERα and ERβ) trigger
opposite pathways which drive E2 target cells to proliferation (via ERα) or apoptosis (via ERβ). Recently, we
identified neuroglobin (NGB) as an E2 inducible heme-protein involved in hormone regulation of cell proliferation
and apoptosis in neuronal and non-neuronal cell lines. In particular, E2 increases NGB protein level
mainly in the mitochondria preventing the release of cytochrome c after an oxidative stress injury. Here, the
mechanisms underlying E2-induced NGB up-regulation, the involvement of signal transduction pathways and
of specific ER subtypes will be discussed in order to propose a possible new E2-dependent scenario at the
root of cell survival and cell death balance.
Keywords: 17 β-estradiol, apoptosis, cell survival, estrogen receptors, neuroglobin.
Rights & PermissionsPrintExport