Astrocytoma cells with elevated levels of RAGE displayed enhanced activity of the proinflammatory nuclear transcription factor kappaB and increased expression of tumor necrosis factor alpha and glial fibrillary acidic protein.
Genes that are susceptible to astrocytic crosstalk between β₂-adrenergic receptors (stimulated by clenbuterol) and TNF-α were identified by qPCR-macroarray-based gene expression analysis in a human 1321 N1 astrocytoma cell line.
These findings thus indicate that sPLA(2)-IIA and TNFalpha transduction pathways interact to modulate inflammatory responses and provide additional insights about the capacity of sPLA(2)-IIA to promote apoptosis resistance in astrocytoma cells.
To study the role of tumor necrosis factor-alpha (TNF-alpha), an important proinflammatory cytokine produced by microglia, on cells overexpressing alpha-synuclein we have used the astrocytoma cell line U373 engineered to express C-terminally truncated alpha-synuclein as a fusion protein with red or green fluorescent proteins.
But the levels of three major BACE mRNA species (7.0, 6.0 and 4.4 kb) were not significantly altered in NTera2-derived neurons, SK-N-SH neuroblastoma or U-373MG astrocytoma following exposure to tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6, interferon-gamma, transforming growth factor-beta1, epidermal growth factor, basic fibroblast growth factor, brain-derived neurotrophic factor, dibutyryl cyclic adenosine monophosphate or phorbol 12-myristate 13-acetate.
We also investigated the expression of nuclear factor-kappa B (NF-kappa B), tumor necrosis factor receptor type 1 (TNFR1), and c-Myc in human astrocytoma tissues in vivo in patients treated with TNF-SAM2 by RT-PCR and immunohistochemical analysis to examine whether there is any correlation between the prognosis of these patients after TNF-SAM2 treatment and the expression of these factors.
Whereas IL-1beta, tumor necrosis factor-alpha, and transforming growth factor-beta mRNA levels remained unchanged, stimulation of astrocytoma cells (T98G, CB193, U118MG) by C3a, C5a, and peptidic C3aR and C5aR agonists induced an increase in the IL-6 mRNA level.
These data show that TNF-alpha produces in astrocytoma cells an early activation of both p38-MAP kinase and JNK, which is followed by the phosphorylation of cPLA2 and the release of AA.
For a better understanding of their pathogenic role, we analyzed signal transduction pathways mediating the interleukin (IL)-1 beta-induced synthesis of IL-6 and tumor necrosis factor alpha (TNF alpha) in the human astrocytoma cell line U373 MG.
We, therefore, examined the expression of IL-6, GM-CSF, and TNF-alpha in human primary astrocytes and astrocytoma cell lines U251 and 253 exposed to IL-1 in serum-free medium.
These data indicate that the bimodal actions of TNF on human astrocytoma cells as well as the stimulatory effects on non-neoplastic adult astrocytes are regulated at least in part by the 55 kDa TNF receptor.
Monocyte-mediated tumoricidal activity, tumor necrosis factor alpha (TNF alpha) secretion and gene expression were examined in astrocytoma patients, patients with other types of brain tumors (primary or metastatic), and normal individuals.