Title : The testosterone metabolite 3α-androstanediol inhibits oxidative stress-induced ERK phosphorylation and neurotoxicity in SH-SY5Y cells through an MKP3/DUSP6-dependent mechanism.

Pub. Date : 2019 Mar 23

PMID : 30552945






5 Functional Relationships(s)
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1 Recently, we demonstrated that 3alpha-diol can protect neurons and neuronal-like cells against oxidative stress-induced neurotoxicity associated with prolonged phosphorylation of the extracellular signal-regulated kinase (ERK). Androstane-3,17-diol mitogen-activated protein kinase 1 Homo sapiens
2 Recently, we demonstrated that 3alpha-diol can protect neurons and neuronal-like cells against oxidative stress-induced neurotoxicity associated with prolonged phosphorylation of the extracellular signal-regulated kinase (ERK). Androstane-3,17-diol mitogen-activated protein kinase 1 Homo sapiens
3 In the present study, we sought to determine whether the ERK-specific phosphatase, mitogen-activated protein kinase phosphatase 3/dual specificity phosphatase 6 (MKP3/DUSP6), is involved in the cytoprotective effects of 3alpha-diol in SH-SY5Y human female neuroblastoma cells. Androstane-3,17-diol mitogen-activated protein kinase 1 Homo sapiens
4 3alpha-diol inhibited ERK phosphorylation and ameliorated cell death induced by the oxidative stressor hydrogen peroxide (H2O2). Androstane-3,17-diol mitogen-activated protein kinase 1 Homo sapiens
5 These findings suggest that the protective effects of 3alpha-diol are mediated through regulation of ERK phosphorylation in neurotoxic conditions and indicate that these effects may be exerted through modulation of MKP3/DUSP6. Androstane-3,17-diol mitogen-activated protein kinase 1 Homo sapiens