{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T14:00:18Z","timestamp":1792159218030,"version":"4.4.0"},"reference-count":56,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2012,1,1]],"date-time":"2012-01-01T00:00:00Z","timestamp":1325376000000},"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":[[2012,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Rationale<\/jats:title>\n                    <jats:p>Sepsis and acute lung injury (ALI) have devastatingly high mortality rates. Both are associated with increased vascular leak, a process regulated by complex molecular mechanisms.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>We hypothesized that integrin \u03b1v\u03b23 could be an important determinant of vascular leak and endothelial permeability in sepsis and ALI.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\u03b23 subunit knockout mice were tested for lung vascular leak after endotracheal LPS, and systemic vascular leak and mortality after intraperitoneal LPS and cecal ligation and puncture. Possible contributory effects of \u03b23 deficiency in platelets and other hematopoietic cells were excluded by bone marrow reconstitution experiments. Endothelial cells treated with \u03b1v\u03b23 antibodies were evaluated for sphingosine-1 phosphate (S1P)\u2013mediated alterations in barrier function, cytoskeletal arrangement, and integrin localization.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>\u03b23 knockout mice had increased vascular leak and pulmonary edema formation after endotracheal LPS, and increased vascular leak and mortality after intraperitoneal LPS and cecal ligation and puncture. In endothelial cells, \u03b1v\u03b23 antibodies inhibited barrier-enhancing and cortical actin responses to S1P. Furthermore, S1P induced translocation of \u03b1v\u03b23 from discrete focal adhesions to cortically distributed sites through Gi- and Rac1-mediated pathways. Cortical \u03b1v\u03b23 localization after S1P was decreased by \u03b1v\u03b23 antibodies, suggesting that ligation of the \u03b1v\u03b23 with its extracellular matrix ligands is required to stabilize cortical \u03b1v\u03b23 focal adhesions.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our studies identify a novel mechanism by which \u03b1v\u03b23 mitigates increased vascular leak, a pathophysiologic function central to sepsis and ALI. These studies suggest that drugs designed to block \u03b1v\u03b23 may have the unexpected side effect of intensifying sepsis- and ALI-associated vascular endothelial leak.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.201108-1381oc","type":"journal-article","created":{"date-parts":[[2011,10,7]],"date-time":"2011-10-07T01:37:05Z","timestamp":1317951425000},"page":"58-66","source":"Crossref","is-referenced-by-count":89,"title":["Absence of Integrin \u03b1v\u03b23 Enhances Vascular Leak in Mice by Inhibiting Endothelial Cortical Actin Formation"],"prefix":"10.1093","volume":"185","author":[{"given":"George","family":"Su","sequence":"first","affiliation":[{"name":"Lung Biology Center, University of California San Francisco, San Francisco, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amha","family":"Atakilit","sequence":"additional","affiliation":[{"name":"Lung Biology Center, University of California San Francisco, San Francisco, 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