{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T23:08:20Z","timestamp":1789945700489,"version":"4.0.1"},"reference-count":63,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2005,4,1]],"date-time":"2005-04-01T00:00:00Z","timestamp":1112313600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2005,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Apolipoprotein J (apoJ; also known as clusterin and sulfated glycoprotein (SGP)\u20102) is associated with senile plaques in degenerating regions of Alzheimer's disease brains, where activated microglia are also prominent. We show a functional link between apoJ and activated microglia by demonstrating that exogenous apoJ activates rodent microglia\n                    <jats:italic>in vivo<\/jats:italic>\n                    and\n                    <jats:italic>in vitro<\/jats:italic>\n                    . Intracerebroventricular infusion of purified human plasma apoJ (\u223c4\u2003\u00b5g over 28\u2003days) activated parenchymal microglia to a phenotype characterized by enlarged cell bodies and processes (phosphotyrosine immunostaining).\n                    <jats:italic>In vitro<\/jats:italic>\n                    , primary rat microglia were also activated by apoJ, with changes in morphology and induction of major histocompatibility complex class II (MHCII) antigen. ApoJ increased the secretion of reactive nitrogen intermediates in a dose\u2010dependent manner (EC\n                    <jats:sub>50<\/jats:sub>\n                    112\u2003n\n                    <jats:sc>m<\/jats:sc>\n                    ), which was completely blocked by aminoguanidine (AG), a nitric oxide synthase inhibitor. However, AG did not block the increased secretion of tumor necrosis factor\u2010\u03b1 by apoJ (EC\n                    <jats:sub>50<\/jats:sub>\n                    55\u2003n\n                    <jats:sc>m<\/jats:sc>\n                    ). Microglial activation by apoJ was also blocked by an anti\u2010apoJ monoclonal antibody (G7), and by chemical cleavage of apoJ with 2\u2010nitro\u20105\u2010thiocyanobenzoate. The mitogen\u2010activated protein kinase kinase and protein kinase C inhibitors PD98059 and H7 inhibited apoJ\u2010mediated induction of reactive nitrogen intermediate secretion from cultured microglia. As a functional measure, apoJ\u2010activated microglia secreted neurotoxic agents in a microglia\u2013neuron co\u2010culture model. We hypothesize that ApoJ contributes to chronic inflammation and neurotoxicity through direct effects on microglia.\n                  <\/jats:p>","DOI":"10.1111\/j.1471-4159.2005.03065.x","type":"journal-article","created":{"date-parts":[[2005,4,27]],"date-time":"2005-04-27T11:22:06Z","timestamp":1114600926000},"page":"1038-1046","source":"Crossref","is-referenced-by-count":51,"title":["Apolipoprotein J (clusterin) activates rodent microglia\n                    <i>in vivo<\/i>\n                    and\n                    <i>in vitro<\/i>"],"prefix":"10.1111","volume":"93","author":[{"given":"Z.","family":"Xie","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. E.","family":"Harris\u2010White","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P. 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