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However, the exact role of OM\u2010MSCs in the GA stress response following cerebral IRI remains to be elucidated. In the present study, we used an oxygen\u2010glucose deprivation\/reoxygenation (OGD\/R) model and reversible middle cerebral artery occlusion (MCAO) model to simulate cerebral IRI in vitro and in vivo. Our results showed that the level of GOLPH3 protein, reactive oxygen species (ROS), and Ca<jats:sup>2+<\/jats:sup> was upregulated, SPCA1 level was downregulated, and GA fragmentation was increased in ischemic stroke models, and OM\u2010MSC treatment clearly ameliorated these GA stress responses in vitro and in vivo. Subsequently, the knockdown of PEDF in OM\u2010MSCs using <jats:italic>PEDF<\/jats:italic>\u2010specific siRNA further demonstrated that secretion of PEDF in OM\u2010MSCs protected OGD\/R\u2010treated N2a cells and MCAO rats from GA stress response. Additionally, rescue experiment using specific pathway inhibitors suggested that OM\u2010MSCs could promote the phosphorylation of the PI3K\/Akt\/mTOR pathway, thereby mitigating OGD\/R\u2010induced GA stress response and excessive autophagy. In conclusion, OM\u2010MSCs minimized the GA stress response following cerebral IRI, at least partially, through the PEDF\u2010PI3K\/Akt\/mTOR pathway.<\/jats:p>","DOI":"10.1155\/2021\/4805040","type":"journal-article","created":{"date-parts":[[2021,11,13]],"date-time":"2021-11-13T19:05:08Z","timestamp":1636830308000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["OM\u2010MSCs Alleviate the Golgi Apparatus Stress Response following Cerebral Ischemia\/Reperfusion Injury via the PEDF\u2010PI3K\/Akt\/mTOR Signaling 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