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For the first time, we present data showing that exposure of rat oligodendrocyte precursor cells (OPCs) to cobalt chloride (CoCl<jats:sub>2<\/jats:sub>), antimycin A (AA), or oxygen, glucose and nutrient deprivation (OGND) causes up\u2010regulation of glucose\u2010regulated protein 78\/B\u2010cell immunoglobulin\u2010binding protein (Grp78\/BiP), C\/EBP homologous binding protein (CHOP), and spliced X\u2010box\u2010binding protein 1 (XBP1). To mimic the effects of ischemia, OPCs supplemented with 5% normal growth medium and 95% Hank's balanced salt solution were incubated in a hypoxia chamber set at 0.1% oxygen. Because the toxic effects of AA on OPCs more closely resembled those seen when OPCs were subjected to OGND, we found AA treatment preferable to CoCl<jats:sub>2<\/jats:sub> as an in vitro model. To investigate the role of XBP1 in survival following an ischemic insult, we generated a stable XBP1 knockdown OPC cell line and subjected it to simulated hypoxia or ischemia. Surprisingly, 65% XBP1 knockdown had no effect on viability following chemical treatment or OGND. These data strengthen the case for targeting the ER stress signalling pathway in an effort to develop new early treatments for ischemic stroke patients but at the same time demonstrate that partial knockdown of XBP1 is not sufficient to protect precursor oligodendrocytes from ischemic damage. \u00a9 2011 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.22583","type":"journal-article","created":{"date-parts":[[2011,2,17]],"date-time":"2011-02-17T16:31:58Z","timestamp":1297960318000},"page":"661-673","source":"Crossref","is-referenced-by-count":9,"title":["Partial XBP1 knockdown does not affect viability of oligodendrocyte precursor cells exposed to new models of hypoxia and ischemia in 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