{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,12]],"date-time":"2026-02-12T15:32:08Z","timestamp":1770910328612,"version":"3.50.1"},"reference-count":58,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2014,8,1]],"date-time":"2014-08-01T00:00:00Z","timestamp":1406851200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2014,8,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>The underlying mechanisms that lysosomal acid lipase (LAL) deficiency causes infiltration of myeloid-derived suppressor cells (MDSCs) in multiple organs and subsequent inflammation remain incompletely understood. Endothelial cells (ECs), lining the inner layer of blood vessels, constitute barriers regulating leukocytes transmigration to the site of inflammation. Therefore, we hypothesized that ECs are dysfunctional in LAL-deficient (lal\u2212\/\u2212) mice. We found that Ly6G+ cells transmigrated more efficiently across lal\u2212\/\u2212 ECs than wild-type (lal+\/+) ECs, which were associated with increased levels of PECAM-1 and MCP-1 in lal\u2212\/\u2212 ECs. In addition, lal\u2212\/\u2212 ECs showed enhanced migration and proliferation, decreased apoptosis, but impaired tube formation and angiogenesis. lal\u2212\/\u2212 ECs also suppressed T cell proliferation in vitro. Interestingly, lal\u2212\/\u2212 Ly6G+ cells promoted in vivo angiogenesis (including a tumor model), EC tube formation, and proliferation. Finally, the mammalian target of rapamycin (mTOR) pathway was activated in lal\u2212\/\u2212 ECs, and inhibition of mTOR reversed EC dysfunctions, including decreasing Ly6G+ cell transmigration, delaying migration, and relieving suppression of T cell proliferation, which was mediated by decreasing production of reactive oxygen species. Our results indicate that LAL regulates EC functions through interaction with MDSCs and modulation of the mTOR pathway, which may provide a mechanistic basis for targeting MDSCs or mTOR to rejuvenate EC functions in LAL deficiency\u2013related diseases.<\/jats:p>","DOI":"10.4049\/jimmunol.1301941","type":"journal-article","created":{"date-parts":[[2014,7,8]],"date-time":"2014-07-08T04:18:04Z","timestamp":1404793084000},"page":"1942-1953","source":"Crossref","is-referenced-by-count":20,"title":["Myeloid-Derived Suppressor Cells Are Involved in Lysosomal Acid Lipase Deficiency\u2013Induced Endothelial Cell Dysfunctions"],"prefix":"10.1093","volume":"193","author":[{"given":"Ting","family":"Zhao","sequence":"first","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Indiana University School of Medicine , Indianapolis, IN 46202"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xinchun","family":"Ding","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Indiana University School of Medicine , Indianapolis, IN 46202"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hong","family":"Du","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Indiana University School of Medicine , Indianapolis, IN 46202"},{"name":"Indiana University Melvin and Bren Simon Cancer Center, Indiana University School of Medicine , Indianapolis, IN 46202"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Cong","family":"Yan","sequence":"additional","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Indiana University School of Medicine , Indianapolis, IN 46202"},{"name":"Indiana University Melvin and Bren Simon Cancer Center, Indiana University School of Medicine , Indianapolis, IN 46202"},{"name":"Center for Immunobiology, Indiana University School of Medicine , Indianapolis, IN 46202"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2014,8,15]]},"reference":[{"key":"2025030707283788100_r1","doi-asserted-by":"crossref","first-page":"L801","DOI":"10.1152\/ajplung.00335.2003","article-title":"Lysosomal acid lipase deficiency causes respiratory inflammation and destruction in the lung","volume":"286","author":"Lian","year":"2004","journal-title":"Am. 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