Apoptosis, of neurons

Xu Y, Kulkosky J, Acheampong E, Nunnari G, Sullivan J, Pomerantz RJ (2004) HIV-l-mediated apoptosis of neuronal cells proximal molecular mechanisms of HIV-l-induced encephalopathy. Proc Natl Acad Sci U S A 101 7070-7075... 

Xu, Y. et al., HIV-1-mediated apoptosis of neuronal cells Proximal molecular mechanisms of HIV-1-induced encephalopathy, Proc. Natl. Acad. Sci. U SA, 101, 7070, 2004. 

A specific cause of apoptosis of neurons is failure to control the concentration of the neurotransmitter glutamate. It is... 

Overexpression of PKC in U937 histiocytic lymphoma cells increased expression of PKCa and p isoforms. In response to TPA, parental U937 cells displayed growth arrest and differentiated into a monocyte/macrophage-like cell line, while PKC overexpressing cells underwent death. The abUity of GF109203X to inhibit TPA-induced cell death suggested that activation of a conventional isoform was necessary to induce apoptosis (de Vente et al., 1995). Activation of PKC enhanced and down-modulation of PKC activity reduced apoptosis of neuronal cells (Mailhos et al., 1994). Ceramide, an activator of PKC is an inducer of apoptosis (Muller et al, 1995 Hannun, 1998, Obeid et al., 1993). 

Measurement of cytochrome c revealed that TNF-a significantly increased the cytosolic cytochrome c levels in PC-12 cells at 6 h (Fig. (10)). The increase in cytochrome c was suppressed to near the control level by the presence of 1 or 10 pM crocin. Therefore, our present results show the possibility that crocin has a pharmacological effect that prevents apoptosis of neuronal cells [17]. 

A. Boldyrev et al.. Effect of carnosine and its natural derivatives on apoptosis of neurons induced by excitotoxic compounds. In Y. Shimonishi (ed.). Peptide science - Present and Future. Springer, Osaka, 1998, pp. 424-426. 

A large family of cysteine proteases has been identified as responsible for apoptosis of neuronal cells. Activation of caspase-3 in CNS was observed in stroke, spinal cord trauma, head injury, and AD and proposed as a target of... 

However, in NGF deprivation-induced apoptosis of neurons, c-myc expression is not correlated with apoptosis (Martin et al., 1992). 

Central among the toxic responses to oxidative stress is the induction of apop-totic death (Curtin et al, 2002 Fleury et al, 2002 Polster and Fkskum, 2004 Ryter et al, 2007). While it is clear that it can be an initiator as well as a signaling event within the apoptotic process, the specific mechanisms underlying these remain uncertain. Likely, these responses could be related to the damage of cellular components e.g. DNA, lipids, and polysaccharides. One potential pathway by which ethanol-mediated oxidative stress may elicit apoptosis of neurons is associated with the oxidation of polyunsaturated fatty acids within mitochondria (Ramachandran et al, 2001, 2003). Among the variety of oxidation products of these fatty acids are toxic/pro-apoptotic aldehydes, the most potent being 4-hydrox-ynonenal (Esterbauer et al, 1990 Uchida et al., 1993). This compound readily induces apoptotic death of neurons (Lovell and Markesbery, 2006 Dwivedi et al., 2007) and is produced in neurons secondary to ethanol-related oxidative stress (Ramachandran et al, 2001, 2003)... 

---