Depletion of intracellular zinc induces apoptosis of cultured hippocampal neurons through suppression of ERK signaling pathway and activation of caspase-3

Influence of Intracellular Zinc on Cultures of Rat Cardiac Neural Crest Cells

“…We also examined cNCC for evidence of apoptosis. As reported by others (Chimienti et al, 2001;Corniola et al, 2008;Bozym et al, 2010;Pang et al, 2012Pang et al, , 2013Strand et al, 2013), cleaved capase-3 (active caspase) was increased significantly in TPEN-treated cNCC. Zn is an endogenous inhibitor of CC3; removal of Zn from procaspase inhibitory binding sites results in the auto-proteolytic cleavage transformation of the zymogen into an active effector capase3 (Peterson et al, 2009;Daniel et al, 2014).…”

“…The disruption of this small readily exchangeable Zn pool has been shown to influence select signaling transduction pathways and/or transcription factors nuclear translocation through the modulation of cellular protein tyrosine phosphatases activity (Brautigan et al, 1981;Haase and Maret, 2005;Wilson et al, 2012), or a disruption of microtubule filaments (Mackenzie and Oteiza, 2007;Mackenzie et al, 2011). Hence, modulation of AKT, ERK, or PKC phosphorylation status, and NFAT, NFkB, AP-1 DNA binding activities has been reported in response to Zn deficiency both in cell culture models and in fetal tissues (Chou et al, 2004;Clegg et al, 2005;Mackenzie et al, 2006a;Mackenzie and Oteiza, 2007;Shen et al, 2008;Aimo et al, 2010;Pang et al, 2013;Nuttall and Oteiza, 2014;Plum et al, 2014). Given the above, changes in cNCC redox status and viability could have been secondary to a disruption of many cellular transducers.…”

Gestational marginal zinc deficiency impaired fetal neural progenitor cell proliferation by disrupting the ERK1/2 signaling pathway

“…In a previous study, we observed that decreased ERK1/2 phosphorylation resulting from zinc deficiency in IMR-32 neuroblastoma is associated with cell cycle arrest and apoptosis [15]. Likewise, apoptotic cell death is associated with decreased ERK1/2 phosphorylation following depletion of intracellular zinc by 24-h exposure to the cell permeable zinc chelator N,N,N′,N′-tetrakis (2-pyridylmethyl) ethylenediamine in cultured hippocampal neurons [24]. Here we report that the inhibition of PP2A in zinc-deficient neuroblastoma cells: (i) rescues ERK1/2 phosphorylation and cell proliferation, but (ii) does not prevent the increased DNA fragmentation and membrane permeability.…”

<em>Akebia quinata</em> Extract Combined with Korean Traditional Juice Activates Antioxidant Enzymes and Reduces Apoptosis and Inflammation

“…Our study demonstrated that the AS-treated group decreased AKT in the alcoholic liver. In cultured hippocampal neurons and endothelial cells, enhancement in activated ERK have been shown to orchestrated the inhibition of apoptosis, preventing the loss of activated ERK, which may be a mechanism by which AQ extracts inhibit ethanol-induced apoptosis [25]. We found that the ethanol-treated group inhibited the phosphorylation of ERK.…”