Expression of the 75 kDA TNF receptor and its role in contact-mediated neuronal cell death

Sipe, Kimberly J.; Dantzer, Robert; Kelley, Keith W.; Weyhenmeyer, James A.

doi:10.1016/s0169-328x(98)00221-6

Cited by 22 publications

(16 citation statements)

References 42 publications

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“…FGF has been shown to upregulate the mRNA for TNFR2 in articular cartilage (Alsalameh et al, 1999) and in C6 glioma cells (Huang et al, 1998). The interaction between membrane-associated TNF␣ and TNFR2 can potentiate cell death in the N1E-15 neuronal cell line (Sipe et al, 1998). In primary microvascular endothelial cells, both TNFR1 and TNFR2 are required for direct TNF-induced apoptosis (Horie et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

“…Expression of Fas, FasL, TNF␣, and the TNF receptors (TNFR1 and TNFR2) has been demonstrated in the CNS and specifically in neurons during development (Sipe et al, 1996(Sipe et al, , 1998Cheema et al, 1999). We have shown previously that Fas mRNA is induced in H19-7 cells after the switch from serum-containing proliferation medium to N2 medium (Gomes et al, 1999).…”

Section: Fasl Tnf␣ and Tnfr Expression At The Mrna Levelmentioning

confidence: 94%

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FGF Induces a Switch in Death Receptor Pathways in Neuronal Cells

et al. 2001

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Basic fibroblast growth factor (FGF2) has many roles in neuronal development and maintenance including effects on mitogenesis, survival, fate determination, differentiation, and migration. Using a conditionally immortalized rat hippocampal cell line, H19-7, and primary hippocampal cultures, we now demonstrate that FGF2 treatment differentially regulates members of the tumor necrosis factor (TNF) superfamily of death domain receptors and their ligands. H19-7 cells transferred from serum to defined (N2) medium undergo apoptosis by a Fas-dependent mechanism similar to primary neurons. In contrast, H19-7 cells treated with FGF undergo apoptosis by a Fas-independent mechanism. FGF suppresses the Fas death pathway but also induces apoptosis by activation of a TNF␣ death pathway in both H19-7 and hippocampal progenitor cells. Expression of the TNF receptor 1 (TNFR1) or TNFR2 in H19-7 cells is sufficient to sensitize the cells to TNF␣, similar to the effects of FGF. Because TNF␣ can be either proapoptotic or antiapoptotic, these results provide an explanation for the divergent trophic effects of FGF2 treatment and the observation that multiple trophic inputs are required for the survival of specific neurons.

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Section: Discussionmentioning

confidence: 99%

Section: Fasl Tnf␣ and Tnfr Expression At The Mrna Levelmentioning

confidence: 94%

FGF Induces a Switch in Death Receptor Pathways in Neuronal Cells

et al. 2001

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Section: Methodsmentioning

confidence: 99%

Curcumin Protects against 1-Methyl-4-phenylpyridinium Ion- and Lipopolysaccharide-Induced Cytotoxicities in the Mouse Mesencephalic Astrocyte via Inhibiting the Cytochrome P450 2E1

Gui

Chen

Peng

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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Curcumin is extracted from the rhizomes of the ginger family plant Curcuma longa L., which has a good protection for liver, kidney, and immune system. However, there is little information about its contribution in protection of astrocytes recently. The present study was undertaken to elucidate the protective effect of curcumin, an herbal antioxidant, on 1-methyl-4-phenylpyridinium ion- (MPP+-) and lipopolysaccharide- (LPS-) induced cytotoxicities, as well as the underlying mechanisms by using primary mouse mesencephalic astrocytes. The results showed that curcumin protected the mesencephalic astrocytes from MPP+- and LPS-induced toxicities along with reducing reactive oxygen species (P < 0.05) and maleic dialdehyde (P < 0.05) sufficiently. Moreover, curcumin significantly inhibited the cytochrome P450 2E1 (CYP2E1) expression (P < 0.01 at mRNA level, P < 0.05 at protein level) and its activity (P < 0.05) sufficiently induced by MPP+ and LPS in the mouse mesencephalic astrocytes. And curcumin as well as diallyl sulphide, a CYP2E1 positive inhibitor, ameliorated MPP+- and LPS-induced mouse mesencephalic astrocytes damage. Accordingly, curcumin protects against MPP+- and LPS-induced cytotoxicities in the mouse mesencephalic astrocyte via inhibiting the CYP2E1 expression and activity.

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“…The absorbance was measured at 570 nm using an Automated Microplated Reader ELx800 (BioTek). The cytotoxicity assessment was exhibited by cytotoxicity index, which was calculated as previously described (Sipe et al, 1998). The morphological changes were observed before adding MTT and images were taken under an inverted light microscope (Nikon, Japan, 22°C).…”

Section: Methodsmentioning

confidence: 99%

Aquaporin-4 knockout enhances astrocyte toxicity induced by 1-methyl-4-phenylpyridinium ion and lipopolysaccharide via increasing the expression of cytochrome P4502E1

et al. 2010

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The role of aquaporin-4 (AQP4) in the regulation of astrocytes function has been widely investigated. However, there is little information about its contribution to the drug metabolism enzymes such as Cytochrome P4502E1. In the present study, we investigated whether AQP4 is involved in the process of the cell damage caused by MPP + and LPS through regulating the expression of CYP2E1 in astrocytes. Compared to the wild-type, in primary astrocytes, AQP4 knockout increased the cell damage and the reactive oxygen species (ROS) production which were induced by MPP + , LPS and ethanol. Notably, AQP4 knockout enhanced the up-regulation of the expression of CYP2E1 in astrocytes exposed to MPP + , LPS and ethanol. Furthermore, Diallylsulphide (DAS), a CYP2E1 inhibitor, partially or almost abolished the cell injury and the ROS production of the astrocytes induced by MPP + and LPS. These findings indicate AQP4 protects astrocytes from the damage caused by MPP + and LPS through reducing the ROS production correlation to the diminished expression of CYP2E1.

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Expression of the 75 kDA TNF receptor and its role in contact-mediated neuronal cell death

Cited by 22 publications

References 42 publications

FGF Induces a Switch in Death Receptor Pathways in Neuronal Cells

FGF Induces a Switch in Death Receptor Pathways in Neuronal Cells

Curcumin Protects against 1-Methyl-4-phenylpyridinium Ion- and Lipopolysaccharide-Induced Cytotoxicities in the Mouse Mesencephalic Astrocyte via Inhibiting the Cytochrome P450 2E1

Aquaporin-4 knockout enhances astrocyte toxicity induced by 1-methyl-4-phenylpyridinium ion and lipopolysaccharide via increasing the expression of cytochrome P4502E1

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