Short communicationBCL-2 blocks glutamate toxicity in neural cell lines
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Cited by (94)
Neuroprotective effect of steroidal alkaloids on glutamate-induced toxicity by preserving mitochondrial membrane potential and reducing oxidative stress
2014, Journal of Steroid Biochemistry and Molecular BiologyCitation Excerpt :Previous studies have reported that neuroprotection mediated through α7-nAChR [52] is correlated with the activation of PI3K and Erk 1/2 pathways. PI3K in turn, phosphorylates Akt [53] and up-regulates the expression of Bcl-2, an anti-apoptotic protein that protects cells from a variety of toxic insults, including glutamate [54]. The cytoprotective effect of Bcl-2 may be due to its ability to modify the cell's Ca2+ homeostasis, particularly by reducing the depletion of Ca2+ from its endoplasmic reticulum store [55].
Dysequilibrium of neuronal proliferation and apoptosis in a pharmacological animal model of psychosis
2012, MethodsCitation Excerpt :However, none of these post mortem and imaging studies could differentiate between necrotic or apoptotic neurodegeneration and the role of neuronal proliferation. The first study directly addressing this issue was published by Jarskog et al. [43], who reported decreased levels of the antiapoptotic and neuroprotective [44,45] regulatory protein bcl-2 in post mortem temporal lobe brain tissue from schizophrenic patients, which clearly parallels the data on bcl-2 in our animal model. Subsequently, the same group reported an enhanced Bax/bcl-2 ratio [46], a feature schizophrenia seems to share with Down’s syndrome, another condition under which excessive apoptosis seems to play an important role [47].
2-Decenoic acid ethyl ester, a derivative of unsaturated medium-chain fatty acids, facilitates functional recovery of locomotor activity after spinal cord injury
2010, NeuroscienceCitation Excerpt :This activity of DAEE would be responsible for the acceleration of functional recovery after injury. Intervention at the level of bcl-2 in the apoptotic pathway is potentially advantageous (Yukawa et al., 2002), because the expression of bcl-2 has been demonstrated to prevent neurons from undergoing cell death induced by a variety of insults that promote apoptosis, including free radicals (Kane et al., 1993), hypoxia (Zhong et al., 1993b), and glutamate toxicity (Zhong et al., 1993a; Kane et al., 1995). In fact, several studies demonstrated that bcl-2 over-expression reduces the neural tissue loss in animal models of spinal cord injury (Lou et al., 1998; Takahashi et al., 1999; Shibata et al., 2000; Seki et al., 2003).
Multiple neuroprotective mechanisms of minocycline in autoimmune CNS inflammation
2007, Neurobiology of DiseaseCitation Excerpt :As revealed by Western blot analysis in our present study, minocycline acts on these two crucial members of the Bcl-2 family by inducing a shift towards the anti-apoptotic side: the expression of Bax was decreased under minocycline treatment whereas the Bcl-2 expression in RGCs was up-regulated. Since it has been demonstrated that glutamate-induced toxicity can result in a down-regulation of Bcl-2 and an increased expression of Bax in the affected neurons (Zhong et al., 1993; Wang et al., 1997; Schelman et al., 2004), the minocycline-induced shift in the Bcl-2 family observed in our study might be secondary to its lowering effect on retinal glutamate concentration. In accordance with this hypothesis, subtoxic amounts of glutamate have been shown to protect neurons by increasing the expression of Bcl-2 as well as activating the MAPK pathway via stimulating the secretion of brain-derived neurotrophic factor (Zhu et al., 2005).