{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T10:30:45Z","timestamp":1784716245812,"version":"3.55.0"},"reference-count":87,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2013,4,19]],"date-time":"2013-04-19T00:00:00Z","timestamp":1366329600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2013,8]]},"abstract":"<jats:p>\n                    The signaling molecule adenosine has been implicated in attenuating acute lung injury (ALI). Adenosine signaling is terminated by its uptake through equilibrative nucleoside transporters (ENTs). We hypothesized that ENT\u2010dependent adenosine uptake could be targeted to enhance adenosine\u2010mediated lung protection. To address this hypothesis, we exposed mice to high\u2010pressure mechanical ventilation to induce ALI. Initial studies demonstrated time\u2010dependent repression of ENT1 and ENT2 transcript and protein levels during ALI. To examine the contention that ENT repression represents an endogenous adaptive response, we performed functional studies with the ENT inhibitor dipyridamole. Dipyridamole treatment (1 mg\/kg; EC\n                    <jats:sub>50<\/jats:sub>\n                    =10 \u03bcM) was associated with significant increases in ALI survival time (277\n                    <jats:italic>vs.<\/jats:italic>\n                    395 min;\n                    <jats:italic>P<\/jats:italic>\n                    &lt;0.05). Subsequent studies in gene\u2010targeted mice for\n                    <jats:italic>Ent1<\/jats:italic>\n                    or\n                    <jats:italic>Ent2<\/jats:italic>\n                    revealed a selective phenotype in\n                    <jats:italic>Ent2<\/jats:italic>\n                    <jats:sup>\u2010\/\u2010<\/jats:sup>\n                    mice, including attenuated pulmonary edema and improved gas exchange during ALI in conjunction with elevated adenosine levels in the bronchoalveolar fluid. Furthermore, studies in genetic models for adenosine receptors implicated the A\n                    <jats:sub>2B<\/jats:sub>\n                    adenosine receptor (Adora2b) in mediating ENT\u2010dependent lung protection. Notably, dipyridamole\u2010dependent attenuation of lung inflammation was abolished in mice with alveolar epithelial\n                    <jats:italic>Adora2b<\/jats:italic>\n                    gene deletion. Our newly identified crosstalk pathway between ENT2 and alveolar epithelial Adora2b in lung protection during ALI opens possibilities for combined therapies targeted to this protein set.\u2014Eckle, T., Hughes, K., Ehrentraut, H., Brodsky, K. S., Rosenberger, P., Choi, D.\u2010S., Ravid, K., Weng, T., Xia, Y., Blackburn, M. R.Eltzschig, H. K., Crosstalk between the equilibrative nucleoside transporter ENT2 and alveolar Adora2b adenosine receptors dampens acute lung injury. FASEB J. 27, 3078\u20133089 (2013).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.13-228551","type":"journal-article","created":{"date-parts":[[2013,4,19]],"date-time":"2013-04-19T22:49:58Z","timestamp":1366411798000},"page":"3078-3089","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":95,"title":["Crosstalk between the equilibrative nucleoside transporter ENT2 and alveolar Adora2b adenosine receptors dampens acute lung injury"],"prefix":"10.1096","volume":"27","author":[{"given":"Tobias","family":"Eckle","sequence":"first","affiliation":[{"name":"Mucosal Inflammation Program Department of Anesthesiology University of Colorado School of Medicine Aurora Colorado 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