Tumor necrosis factor α augments amyloid β protein (25–35) induced apoptosis in human cells

• Published in: Neuroscience letters Vol. 238; no. 1; pp. 17 - 20
• Main Authors: Blasko, I, Schmitt, T.L, Steiner, E, Trieb, K, Grubeck-Loebenstein, B
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 28-11-1997; Elsevier
• Subjects: Alzheimer's disease; Amyloid beta-Peptides - pharmacology; Amyloid β protein; Amyloid β protein (25–35); Apoptosis; Biological and medical sciences; Cells, Cultured; Culture Media, Serum-Free; Cytokines; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases; DU-145; Humans; Kidney - pathology; Kidney cells; Male; Medical sciences; Neuroblastoma - pathology; Neurology; Peptide Fragments - pharmacology; Prostatic Neoplasms - pathology; SK-N-SH; Species Specificity; Thyroid cells; Thyroid Gland - pathology; Tumor Cells, Cultured; Tumor necrosis factor α; Tumor Necrosis Factor-alpha - pharmacology; Amyloid β protein; Amyloid β protein (25–35); Cytokines; Thyroid cells; SK-N-SH; DU-145; Kidney cells; Alzheimer's disease; Tumor necrosis factor α; Apoptosis; Human; Nervous system diseases; Alzheimer disease; Cytokine; In vitro; Cerebral disorder; Cell line; Cell death; β Amyloid protein; Central nervous system disease; Degenerative disease
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/S0304-3940(97)00845-8

No information is yet available on the effect of tumor necrosis factor
α (TNF
α) on amyloid
β protein (A
β)-induced cytotoxicity in human cells. For this reason the induction of apoptosis by TNF
α and A
β (25–35) was studied in primary cultures of human thyroid and kidney cells as well as in the neuroblastoma line SK-N-SH and in DU-145 cells. Apoptosis occurred in all cell types after A
β (25–35) treatment, but was markedly enhanced when TNF
α was additionally present. This effect was less pronounced in transformed cell lines than in primary cultures, in which TNF
α on its own was not cytotoxic. Apoptosis was still more prevalent under serum free culture conditions. The results demonstrate that TNF
α may support the occurrence of A
β-mediated cell death and thus contribute to the development of pathological changes in Alzheimer's disease (AD).