title: Intercellular signaling initiated by nitric oxide produced in heat-shocked human glioblastoma cells.
abstract: The accumulation of inducible nitric oxide synthase was caused by heat shock of human glioblastoma T98G cells but not of A-172 cells. The accumulation of hsp72 and p53 was observed in A-172 cells cocultivated with heat-shocked T98G cells, which was suppressed by the addition of aminoguanidine to the medium. The accumulation of these proteins was observed in A-172 cells after exposure to the conditioned medium of heat-shocked T98G cells, which was completely blocked by the addition of 2-(4-carboxyphenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide to the medium. In addition, the accumulation of these proteins in A-172 cells was induced by the administration of S-nitroso-N-acetylpenicillamine to the medium. Finally, the thermosensitivity of A-172 cells was reduced in the conditioned medium of heat-shocked T98G cells compared with conventional fresh growth medium. Our findings demonstrate that the accumulation of stress-induced proteins and thermoresistance in NO recipient cells cocultivated with heat-shocked NO donor cells is induced through an intercellular signal transduction pathway initiated by NO without cell-to-cell interactions such as gap junctions.
authors.affiliation: Department of Experimental Radiology and Health Physics, Fukui Medical University, Matsuoka, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Matsumoto
authors.forename: S
authors.initials: S
authors.lastname: Hayashi
authors.forename: M
authors.initials: M
authors.lastname: Hatashita
authors.forename: H
authors.initials: H
authors.lastname: Shioura
authors.forename: T
authors.initials: T
authors.lastname: Ohtsubo
authors.forename: R
authors.initials: R
authors.lastname: Kitai
authors.forename: T
authors.initials: T
authors.lastname: Ohnishi
authors.forename: E
authors.initials: E
authors.lastname: Kano
mesh_terms: D001932:Brain Neoplasms / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D003470:Culture Media; D005909:Glioblastoma / Q000201:enzymology / Q000378:metabolism* / Q000473:pathology; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000378:metabolism; D018869:Heat-Shock Response; D006801:Humans; D009569:Nitric Oxide / Q000502:physiology*; D020030:Nitric Oxide Donors / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II; D009573:Nitrites / Q000378:metabolism; D010396:Penicillamine / Q000031:analogs & derivatives / Q000494:pharmacology; D026423:S-Nitroso-N-Acetylpenicillamine; D015398:Signal Transduction / Q000502:physiology*; D014407:Tumor Cells, Cultured; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism
chemical_list: D003470:Culture Media; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D020030:Nitric Oxide Donors; D009573:Nitrites; D016159:Tumor Suppressor Protein p53; D009569:Nitric Oxide; D026423:S-Nitroso-N-Acetylpenicillamine; C496319:NOS2 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D010396:Penicillamine