{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T19:36:43Z","timestamp":1785785803840,"version":"3.56.0"},"reference-count":29,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2018,2,6]],"date-time":"2018-02-06T00:00:00Z","timestamp":1517875200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["K08HL129080"],"award-info":[{"award-number":["K08HL129080"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007520","name":"Nationwide Children's Hospital","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100007520","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2018,6]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>The L\u2010arginine\/<jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content> pathway is an important regulator of pulmonary hypertension, the leading cause of mortality in patients with the chronic lung disease of prematurity, bronchopulmonary dysplasia. L\u2010arginine can be metabolized by <jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content> synthase (<jats:styled-content style=\"fixed-case\">NOS<\/jats:styled-content>) to form L\u2010citrulline and <jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content>, a potent vasodilator. Alternatively, L\u2010arginine can be metabolized by arginase to form urea and L\u2010ornithine, a precursor to collagen and proline formation important in vascular remodelling. In the current study, we hypothesized that C3H\/HeN mice exposed to prolonged hyperoxia would have increased arginase expression and pulmonary vascular wall cell proliferation. C3H\/HeN mice were exposed to 14\u00a0days of 85% O<jats:sub>2<\/jats:sub> or room air and lung homogenates analyzed by western blot for protein levels of arginase I, arginase <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content>, endothelial <jats:styled-content style=\"fixed-case\">NOS<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">eNOS<\/jats:styled-content>), ornithine decarboxylase (<jats:styled-content style=\"fixed-case\">ODC<\/jats:styled-content>), ornithine aminotransferase (<jats:styled-content style=\"fixed-case\">OAT<\/jats:styled-content>), and \u03b1\u2010smooth muscle actin (\u03b1\u2010<jats:styled-content style=\"fixed-case\">SMA<\/jats:styled-content>). Hyperoxia did not change arginase I or <jats:styled-content style=\"fixed-case\">eNOS<\/jats:styled-content> protein levels. However, arginase <jats:styled-content style=\"fixed-case\">II<\/jats:styled-content> protein levels were 15\u2010fold greater after hyperoxia exposure than in lungs exposed to room air. Greater protein levels of <jats:styled-content style=\"fixed-case\">ODC<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">OAT<\/jats:styled-content> were found in lungs following hyperoxic exposure than in room air animals. \u03b1\u2010<jats:styled-content style=\"fixed-case\">SMA<\/jats:styled-content> protein levels were found to be 7\u2010fold greater in the hyperoxia exposed lungs than in room air lungs. In the hyperoxia exposed lungs there was evidence of greater pulmonary vascular wall cell proliferation by \u03b1\u2010<jats:styled-content style=\"fixed-case\">SMA<\/jats:styled-content> immunohistochemistry than in room air lungs. Taken together, these data are consistent with a more proliferative vascular phenotype, and may explain the propensity of patients with bronchopulmonary dysplasia to develop pulmonary hypertension.<\/jats:p>","DOI":"10.1111\/1440-1681.12909","type":"journal-article","created":{"date-parts":[[2017,12,20]],"date-time":"2017-12-20T14:58:13Z","timestamp":1513781893000},"page":"556-562","source":"Crossref","is-referenced-by-count":11,"title":["Arginase and \u03b1\u2010smooth muscle actin induction after hyperoxic exposure in a mouse model of bronchopulmonary dysplasia"],"prefix":"10.1111","volume":"45","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3932-9204","authenticated-orcid":false,"given":"Jennifer K","family":"Trittmann","sequence":"first","affiliation":[{"name":"Pulmonary Hypertension Group Center for Perinatal Research The Research Institute at Nationwide Children's Hospital  Columbus OH USA"},{"name":"Department of Pediatrics The Ohio State University  Columbus OH USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Markus","family":"Velten","sequence":"additional","affiliation":[{"name":"Department of Anesthesiology and Intensive Care Medicine Rheinische Friedrich\u2010Wilhelms University University Medical Center  Bonn Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kathryn M","family":"Heyob","sequence":"additional","affiliation":[{"name":"Pulmonary Hypertension Group Center for Perinatal Research The Research Institute at Nationwide Children's Hospital  Columbus OH USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hanadi","family":"Almazroue","sequence":"additional","affiliation":[{"name":"Pulmonary Hypertension Group Center for Perinatal Research The Research Institute at Nationwide Children's Hospital  Columbus OH USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi","family":"Jin","sequence":"additional","affiliation":[{"name":"Pulmonary Hypertension Group 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