<HashMap><database>biostudies-literature</database><scores/><additional><submitter>De Blasio MJ</submitter><funding>British Heart Foundation</funding><funding>Biotechnology and Biological Sciences Research Council</funding><pagination>e0136115</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4545393</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(8)</volume><pubmed_abstract>The effects of endogenous and synthetic glucocorticoids on fetal lung maturation are well-established, although the role of leptin in lung development before birth is unclear. This study examined mRNA and protein levels of the signalling long-form leptin receptor (Ob-Rb) in fetal ovine lungs towards term, and after experimental manipulation of glucocorticoid levels in utero by fetal cortisol infusion or maternal dexamethasone treatment. In fetal ovine lungs, Ob-Rb protein was localised to bronchiolar epithelium, bronchial cartilage, vascular endothelium, alveolar macrophages and type II pneumocytes. Pulmonary Ob-Rb mRNA abundance increased between 100 (0.69 fractional gestational age) and 144 days (0.99) of gestation, and by 2-4-fold in response to fetal cortisol infusion and maternal dexamethasone treatment. In contrast, pulmonary Ob-Rb protein levels decreased near term and were halved by glucocorticoid treatment, without any significant change in phosphorylated signal transducer and activator of transcription-3 (pSTAT3) at Ser727, total STAT3 or the pulmonary pSTAT3:STAT3 ratio. Leptin mRNA was undetectable in fetal ovine lungs at the gestational ages studied. These findings demonstrate differential control of pulmonary Ob-Rb transcript abundance and protein translation, and/or post-translational processing, by glucocorticoids in utero. Localisation of Ob-Rb in the fetal ovine lungs, including alveolar type II pneumocytes, suggests a role for leptin signalling in the control of lung growth and maturation before birth.</pubmed_abstract><journal>PloS one</journal><pubmed_title>Developmental Expression and Glucocorticoid Control of the Leptin Receptor in Fetal Ovine Lung.</pubmed_title><pmcid>PMC4545393</pmcid><funding_grant_id>S18103</funding_grant_id><funding_grant_id>RG/06/006/22028</funding_grant_id><funding_grant_id>BB/E002668/1</funding_grant_id><funding_grant_id>BB/H01697X/1</funding_grant_id><funding_grant_id>RG/11/16/29260</funding_grant_id><pubmed_authors>Charnock-Jones DS</pubmed_authors><pubmed_authors>Fowden AL</pubmed_authors><pubmed_authors>De Blasio MJ</pubmed_authors><pubmed_authors>Davies KL</pubmed_authors><pubmed_authors>Vaughan OR</pubmed_authors><pubmed_authors>Kempster SL</pubmed_authors><pubmed_authors>Forhead AJ</pubmed_authors><pubmed_authors>Plein A</pubmed_authors><pubmed_authors>Smith GC</pubmed_authors><pubmed_authors>Blache D</pubmed_authors><pubmed_authors>Bernstein BS</pubmed_authors><pubmed_authors>Boije M</pubmed_authors><pubmed_authors>Wooding FB</pubmed_authors><pubmed_authors>Giussani DA</pubmed_authors></additional><is_claimable>false</is_claimable><name>Developmental Expression and Glucocorticoid Control of the Leptin Receptor in Fetal Ovine Lung.</name><description>The effects of endogenous and synthetic glucocorticoids on fetal lung maturation are well-established, although the role of leptin in lung development before birth is unclear. This study examined mRNA and protein levels of the signalling long-form leptin receptor (Ob-Rb) in fetal ovine lungs towards term, and after experimental manipulation of glucocorticoid levels in utero by fetal cortisol infusion or maternal dexamethasone treatment. In fetal ovine lungs, Ob-Rb protein was localised to bronchiolar epithelium, bronchial cartilage, vascular endothelium, alveolar macrophages and type II pneumocytes. Pulmonary Ob-Rb mRNA abundance increased between 100 (0.69 fractional gestational age) and 144 days (0.99) of gestation, and by 2-4-fold in response to fetal cortisol infusion and maternal dexamethasone treatment. In contrast, pulmonary Ob-Rb protein levels decreased near term and were halved by glucocorticoid treatment, without any significant change in phosphorylated signal transducer and activator of transcription-3 (pSTAT3) at Ser727, total STAT3 or the pulmonary pSTAT3:STAT3 ratio. Leptin mRNA was undetectable in fetal ovine lungs at the gestational ages studied. These findings demonstrate differential control of pulmonary Ob-Rb transcript abundance and protein translation, and/or post-translational processing, by glucocorticoids in utero. Localisation of Ob-Rb in the fetal ovine lungs, including alveolar type II pneumocytes, suggests a role for leptin signalling in the control of lung growth and maturation before birth.</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015</publication><modification>2024-11-15T11:45:02.49Z</modification><creation>2019-03-26T23:35:25Z</creation></dates><accession>S-EPMC4545393</accession><cross_references><pubmed>26287800</pubmed><doi>10.1371/journal.pone.0136115</doi></cross_references></HashMap>