{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,3,13]],"date-time":"2025-03-13T04:13:08Z","timestamp":1741839188750,"version":"3.38.0"},"reference-count":36,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2016,8,31]],"date-time":"2016-08-31T00:00:00Z","timestamp":1472601600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2017,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Nitric oxide (<jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content>) deficiency is common in pulmonary diseases, but its effect on pulmonary remodelling is still controversial. As pulmonary parathyroid hormone\u2010related protein (<jats:styled-content style=\"fixed-case\">PTH<\/jats:styled-content>rP) expression is a key regulator of pulmonary fibrosis and development, the effect of chronic <jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content> deficiency on the pulmonary <jats:styled-content style=\"fixed-case\">PTH<\/jats:styled-content>rP system and its relationship with oxidative stress was addressed. <jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content> bioavailability in adult rats was reduced by systemic administration of L\u2010<jats:styled-content style=\"fixed-case\">NAME <\/jats:styled-content><jats:italic>via<\/jats:italic> tap water. To clarify the role of <jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content> synthase (<jats:styled-content style=\"fixed-case\">NOS<\/jats:styled-content>)\u20103\u2010derived <jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content> on pulmonary expression of <jats:styled-content style=\"fixed-case\">PTH<\/jats:styled-content>rP, <jats:styled-content style=\"fixed-case\">NOS<\/jats:styled-content>\u20103\u2010deficient mice were used. Captopril and hydralazine were used to reduce the hypertensive effect of L\u2010<jats:styled-content style=\"fixed-case\">NAME<\/jats:styled-content> treatment and to interfere with the pulmonary renin\u2010angiotensin system (<jats:styled-content style=\"fixed-case\">RAS<\/jats:styled-content>). Quantitative <jats:styled-content style=\"fixed-case\">RT<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content> and immunoblot techniques were used to characterize the expression of key proteins involved in pulmonary remodelling. L\u2010<jats:styled-content style=\"fixed-case\">NAME<\/jats:styled-content> administration significantly reduced pulmonary <jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content> concentration and caused oxidative stress as characterized by increased pulmonary nitrite concentration and increased expression of <jats:styled-content style=\"fixed-case\">NOX<\/jats:styled-content>2, p47phox and p67phox. Furthermore, L\u2010<jats:styled-content style=\"fixed-case\">NAME<\/jats:styled-content> induced the pulmonary expression of <jats:styled-content style=\"fixed-case\">PTH<\/jats:styled-content>rP and of its corresponding receptor, <jats:styled-content style=\"fixed-case\">PTH<\/jats:styled-content>\u20101R. Expression of <jats:styled-content style=\"fixed-case\">PTH<\/jats:styled-content>rP and <jats:styled-content style=\"fixed-case\">PTH<\/jats:styled-content>\u20101R correlated with the expression of two well\u2010established <jats:styled-content style=\"fixed-case\">PTH<\/jats:styled-content>rP downstream targets, <jats:styled-content style=\"fixed-case\">ADRP<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3, suggesting an activation of the pulmonary <jats:styled-content style=\"fixed-case\">PTH<\/jats:styled-content>rP system by <jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content> deficiency. Captopril reduced the expression of <jats:styled-content style=\"fixed-case\">PTH<\/jats:styled-content>rP, profibrotic markers and ornithine decarboxylase, but neither that of <jats:styled-content style=\"fixed-case\">PTH<\/jats:styled-content>\u20101R nor that of <jats:styled-content style=\"fixed-case\">ADRP<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">PPAR<\/jats:styled-content>\u03b3. All transcriptional changes were confirmed in <jats:styled-content style=\"fixed-case\">NOS<\/jats:styled-content>\u20103\u2010deficient mice. In conclusion, <jats:styled-content style=\"fixed-case\">NOS<\/jats:styled-content>\u20103\u2010derived <jats:styled-content style=\"fixed-case\">NO<\/jats:styled-content> suppresses pulmonary <jats:styled-content style=\"fixed-case\">PTH<\/jats:styled-content>rP and <jats:styled-content style=\"fixed-case\">PTH<\/jats:styled-content>\u20101R expression, thereby modifying pulmonary remodelling.<\/jats:p>","DOI":"10.1111\/jcmm.12942","type":"journal-article","created":{"date-parts":[[2016,9,1]],"date-time":"2016-09-01T04:12:44Z","timestamp":1472703164000},"page":"96-106","source":"Crossref","is-referenced-by-count":1,"title":["Effect of nitric oxide deficiency on the pulmonary <scp>PTH<\/scp>rP system"],"prefix":"10.1111","volume":"21","author":[{"given":"Bastian","family":"Brockhoff","sequence":"first","affiliation":[{"name":"Physiologisches Institut Justus\u2010Liebig\u2010Universit\u00e4t Gie\u00dfen Gie\u00dfen 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