Differential modulation of cell death proteins in human brain cells by tumor necrosis factor alpha and platelet activating factor

Pulliam, Lynn; Zhou, Mei; Stubblebine, Marcia; Bitler, Catherine M.

doi:10.1002/(sici)1097-4547(19981115)54:4<530::aid-jnr10>3.0.co;2-1

Cited by 41 publications

(15 citation statements)

References 39 publications

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“…In this study, we showed that PAF up-regulated gene expression and protein synthesis of antiapoptotic factors, such as Bcl-2 and Bcl-xL. Our results are in accordance with the fact that PAF enhances the expression of Bcl-xL in human brain cells (26). However, experiments regarding the influence of PAF on apoptosis had rather ) were pretreated with a PAF antagonist, WEB 2170 (10 Ag/mL), or NF-nB inhibitor, parthenolide (Parth , 5 Amol/L), 30 minutes before PAF (3 Amol/L) treatment.…”

Section: Discussionsupporting

confidence: 89%

Platelet-Activating Factor Induces Up-regulation of Antiapoptotic Factors in a Melanoma Cell Line through Nuclear Factor-κB Activation

Seo

Kim

et al. 2006

Cancer Research

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In this study, we investigated the influence of plateletactivating factor (PAF) on the induction of apoptosisregulating factors in B16F10 melanoma cells. PAF increased the expression of mRNA and the protein synthesis of antiapoptotic factors, such as Bcl-2 and Bcl-xL, but did not increase the expression of the proapoptotic factor, Bax. A selective nuclear factor-KB (NF-KB) inhibitor, parthenolide, inhibited the effects of PAF. Furthermore, PAF inhibited etoposide-induced increases in caspase-3, caspase-8, and caspase-9 activities, as well as cell death. p50/p65 heterodimer increased the mRNA expression of Bcl-2 and Bcl-xL and decreased etoposide-induced caspase activities and cell death.In an in vivo model in which Matrigel was injected s.c., PAF augmented the growth of B16F10 cells and attenuated etoposide-induced inhibition of B16F10 cells growth. These data indicate that PAF induces up-regulation of antiapoptotic factors in a NF-KB-dependent manner in a melanoma cell line, therefore suggesting that PAF may diminish the cytotoxic effect of chemotherapeutic agents. (Cancer Res 2006; 66(9): 4681-6)

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Section: Discussionsupporting

confidence: 89%

Platelet-Activating Factor Induces Up-regulation of Antiapoptotic Factors in a Melanoma Cell Line through Nuclear Factor-κB Activation

Seo

Kim

et al. 2006

Cancer Research

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“…In our system, TNF-a performed protective functions probably by stabilizing the expression of anti-apoptotic protein Bcl-2. It has been recently shown that TNF-a influence on the Bclfamily of proteins might also vary from inhibition to stimulation depending on the cell type and other factors: TNF-a could decrease or slightly increase the expression of Bcl-2 family proteins 41,42 or may enhance the expression of pro-apoptotic protein Bax, 41 though not in all systems. 42 We did not detect any marked change in Bax Figure 4 TNF-a prevents prostate cancer-induced inhibition of Bcl-2 expression in DC.…”

Section: Discussionmentioning

confidence: 99%

TNF-α protects dendritic cells from prostate cancer-induced apoptosis

Pirtskhalaishvili

Shurin

Esche

et al. 2001

Prostate Cancer Prostatic Dis

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We have recently shown that human prostate cancer (PCa) cells induced apoptotic death of the most potent antigen-presenting cells, dendritic cells (DC), which are responsible for the induction of specific antitumor immune responses. Here we have evaluated the effect of murine PCa cells RM-1 on the survival of immature and tumor necrosis factor-a (TNF-a)-stimulated mature DC. PCa cells and DC were co-incubated for 24 -48 h and DC apoptosis was assessed by morphologic criteria, Annexin V assay, and TUNEL staining. We have shown that co-incubation of RM-1 cells with DC is accompanied by an increased level of DC apoptosis, which was mediated by decreased expression of anti-apoptotic protein Bcl-2. Stimulation of DC maturation by TNF-a resulted in increased resistance of DC to PCa-induced apoptosis. In TNF-a treated mature DC, but not in immature DC, the expression of Bcl-2 was not blocked after exposure to RM-1-derived factors. Thus, these data suggest that TNF-a-induced maturation of DC increases their resistance to PCa induced apoptosis. This is likely to be due to the stabilizing of the expression of anti-apoptotic protein Bcl-2. The difference in the sensitivity of mature and immature DC to PCa-induced cell death should be considered during the design of DC-based clinical trials for PCa patients. Prostate Cancer and Prostatic Diseases (2001) 4, 221-227.

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“…60 Under physiological or pathophysiological conditions, Lcysteine can stimulate NMDARs and lead to neuronal apoptosis. 60 TNF-a is capable of stimulating apoptosis in human neurons, 133,134 but an indirect route of injury cannot be excluded. Expression of TNF-a and its receptor are elevated in brains from patients with HAD.…”

Section: Mechanisms Of Neuronal Injury and Death In Hadmentioning

confidence: 99%

HIV-1 infection and AIDS: consequences for the central nervous system

et al. 2005

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Infection with the human immunodeficiency virus-1 (HIV-1) can induce severe and debilitating neurological problems that include behavioral abnormalities, motor dysfunction and frank dementia. After infiltrating peripheral immune competent cells, in particular macrophages, HIV-1 provokes a neuropathological response involving all cell types in the brain. HIV-1 also incites activation of chemokine receptors, inflammatory mediators, extracellular matrix-degrading enzymes and glutamate receptor-mediated excitotoxicity, all of which can trigger numerous downstream signaling pathways and disrupt neuronal and glial function. This review will discuss recently uncovered pathologic neuroimmune and degenerative mechanisms contributing to neuronal damage induced by HIV-1 and potential approaches for development of future therapeutic intervention.

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Differential modulation of cell death proteins in human brain cells by tumor necrosis factor alpha and platelet activating factor

Cited by 41 publications

References 39 publications

Platelet-Activating Factor Induces Up-regulation of Antiapoptotic Factors in a Melanoma Cell Line through Nuclear Factor-κB Activation

Platelet-Activating Factor Induces Up-regulation of Antiapoptotic Factors in a Melanoma Cell Line through Nuclear Factor-κB Activation

TNF-α protects dendritic cells from prostate cancer-induced apoptosis

HIV-1 infection and AIDS: consequences for the central nervous system

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