{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,24]],"date-time":"2026-02-24T08:20:50Z","timestamp":1771921250100,"version":"3.50.1"},"reference-count":44,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2014,2]]},"abstract":"<jats:sec>\n            <jats:title>Objective\u2014<\/jats:title>\n            <jats:p>\n              Transgenic overexpression of the human cysteinyl leukotriene receptor 2 (CysLT\n              <jats:sub>2<\/jats:sub>\n              R) in murine endothelium exacerbates vascular permeability and ischemia\/reperfusion injury. Here, we explore the underlying mechanisms of CysLT\n              <jats:sub>2<\/jats:sub>\n              R activation-mediated inflammation and delineate the relative contributions of endogenous murine CysLT\n              <jats:sub>2<\/jats:sub>\n              R and the transgene-derived receptor.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results\u2014<\/jats:title>\n            <jats:p>\n              We created a novel mouse with only endothelial-expressed CysLT\n              <jats:sub>2<\/jats:sub>\n              R (endothelium-targeted overexpression mice [EC]\/CysLT\n              <jats:sub>2<\/jats:sub>\n              R-knockout mice [KO]) by crossing EC with KO to dissect the role of endothelial CysLT\n              <jats:sub>2<\/jats:sub>\n              R in tissue injury. Surprisingly, we discovered that damage in EC\/KO mice was not elevated (24% versus 47% EC) after ischemia\/reperfusion. We examined vascular permeability and leukocyte recruitment\/rolling responses in the cremaster vasculature after cysteinyl leukotriene (cysLT) stimulation. Mice possessing transgenic endothelial CysLT\n              <jats:sub>2<\/jats:sub>\n              R overexpression, whether EC or EC\/KO, when stimulated with cysLTs, exhibited vascular hyperpermeability, declining leukocyte flux, and a transient increase in slow-rolling leukocyte fraction. Mice lacking endogenous CysLT\n              <jats:sub>2<\/jats:sub>\n              R (both KO [20\u00b13 cells\/min] EC\/KO [24\u00b13]) showed lower-rolling leukocyte flux versus wild-type (38\u00b16) and EC (35\u00b16) mice under unstimulated conditions. EC\/KO mice differed from EC counterparts in that vascular hyperpermeability was not present in the absence of exogenous cysLTs.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\u2014<\/jats:title>\n            <jats:p>\n              These results indicate that endothelial and nonendothelial CysLT\n              <jats:sub>2<\/jats:sub>\n              R niches have separate roles in mediating inflammatory responses. Endothelial receptor activation results in increased vascular permeability and leukocyte slow-rolling, facilitating leukocyte transmigration. Nonendothelial receptors, likely located on resident\/circulating leukocytes, facilitate endothelial receptor activation and leukocyte transit. Activation of both receptor populations is required for injury exacerbation.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.113.302536","type":"journal-article","created":{"date-parts":[[2013,11,28]],"date-time":"2013-11-28T05:09:51Z","timestamp":1385615391000},"page":"321-330","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":20,"title":["Multiple-Site Activation of the Cysteinyl Leukotriene Receptor 2 Is Required for Exacerbation of Ischemia\/Reperfusion Injury"],"prefix":"10.1161","volume":"34","author":[{"given":"Nathan C.","family":"Ni","sequence":"first","affiliation":[{"name":"From the Department of Biomedical and Molecular Sciences (N.C.N., L.L.B., C.D.F.) and Cancer Research Institute (J.D.M.), Queen\u2019s University, Kingston, ON, Canada."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Laurel L.","family":"Ballantyne","sequence":"additional","affiliation":[{"name":"From the Department of Biomedical and Molecular Sciences (N.C.N., L.L.B., C.D.F.) and Cancer Research Institute (J.D.M.), Queen\u2019s University, Kingston, ON, Canada."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeffrey D.","family":"Mewburn","sequence":"additional","affiliation":[{"name":"From the Department of Biomedical and Molecular Sciences (N.C.N., L.L.B., C.D.F.) and Cancer Research Institute (J.D.M.), Queen\u2019s University, Kingston, ON, Canada."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Colin D.","family":"Funk","sequence":"additional","affiliation":[{"name":"From the Department of Biomedical and Molecular Sciences (N.C.N., L.L.B., C.D.F.) and Cancer Research Institute (J.D.M.), Queen\u2019s University, Kingston, ON, 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