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U.S.A."],"published-print":{"date-parts":[[2002,5,28]]},"abstract":"<jats:p>\n                    Prostaglandin D\n                    <jats:sub>2<\/jats:sub>\n                    (PGD\n                    <jats:sub>2<\/jats:sub>\n                    ), a major cyclooxygenase product in a variety of tissues and cells, readily undergoes dehydration to yield the bioactive cyclopentenone-type PGs of the J\n                    <jats:sub>2<\/jats:sub>\n                    -series, such as 15-deoxy-\u0394\n                    <jats:sup>12,14<\/jats:sup>\n                    -PGJ\n                    <jats:sub>2<\/jats:sub>\n                    (15d-PGJ\n                    <jats:sub>2<\/jats:sub>\n                    ). The observation that the level of 15d-PGJ\n                    <jats:sub>2<\/jats:sub>\n                    increased in the tissue cells from patients with sporadic amyotrophic lateral sclerosis suggested that the formation of 15d-PGJ\n                    <jats:sub>2<\/jats:sub>\n                    may be closely associated with neuronal cell death during chronic inflammatory processes.\n                    <jats:italic>In vitro<\/jats:italic>\n                    experiments using SH-SY5Y human neuroblastoma cells revealed that 15d-PGJ\n                    <jats:sub>2<\/jats:sub>\n                    induced apoptotic cell death. An oligonucleotide microarray analysis demonstrated that, in addition to the heat shock-responsive and redox-responsive genes, the p53-responsive genes, such as\n                    <jats:italic>gadd45<\/jats:italic>\n                    ,\n                    <jats:italic>cyclin G1<\/jats:italic>\n                    , and\n                    <jats:italic>cathepsin D<\/jats:italic>\n                    , were significantly up-regulated in the cells treated with 15d-PGJ\n                    <jats:sub>2<\/jats:sub>\n                    . Indeed, the 15d-PGJ\n                    <jats:sub>2<\/jats:sub>\n                    induced accumulation and phosphorylation of p53, which was accompanied by a preferential redistribution of the p53 protein in the nuclei of the cells and by a time-dependent increase in p53 DNA binding activity, suggesting that p53 accumulated in response to the treatment with 15d-PGJ\n                    <jats:sub>2<\/jats:sub>\n                    was functional. The 15d-PGJ\n                    <jats:sub>2<\/jats:sub>\n                    -induced accumulation of p53 resulted in the activation of a death-inducing caspase cascade mediated by Fas and the Fas ligand.\n                  <\/jats:p>","DOI":"10.1073\/pnas.112212599","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:46:49Z","timestamp":1027680409000},"page":"7367-7372","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":142,"title":["15-Deoxy-\u0394\n                    <sup>12,14<\/sup>\n                    -prostaglandin J\n                    <sub>2<\/sub>\n                    : The endogenous electrophile that induces neuronal apoptosis"],"prefix":"10.1073","volume":"99","author":[{"given":"Mitsuhiro","family":"Kondo","sequence":"first","affiliation":[{"name":"Laboratory of Food and Biodynamics, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya 464-8601, Japan; 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