<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chao CM</submitter><funding>Deutsche Forschungsgemeinschaft, DZL, First Affiliated Hospital of Wenzhou Medical University</funding><pagination>E859</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7226730</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>9(4)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Bronchopulmonary dysplasia (BPD) is a lung disease of preterm born infants, characterized by alveolar simplification. MicroRNA (&lt;i>miR)&lt;/i> are known to be involved in many biological and pathological processes in the lung. Although a changed expression has been described for several &lt;i>miR&lt;/i> in BPD, a causal role remains to be established.&lt;h4>Results&lt;/h4>Our results showed that the expression level of &lt;i>miR-154&lt;/i> increases during lung development and decreases postnatally. Further, hyperoxia treatment maintains high levels of &lt;i>miR-154&lt;/i> in alveolar type 2 cells (AT2). We hypothesized that the decrease in &lt;i>miR-154&lt;/i> expression in AT2 cells is required for normal alveologenesis. To test this hypothesis, we generated a novel transgenic mouse allowing doxycycli</pubmed_abstract><journal>Cells</journal><pubmed_title>Failure to Down-Regulate &lt;i>miR-154&lt;/i> Expression in Early Postnatal Mouse Lung Epithelium Suppresses Alveologenesis, with Changes in Tgf-β Signaling Similar to those Induced by Exposure to Hyperoxia.</pubmed_title><pmcid>PMC7226730</pmcid><funding_grant_id>DFG; BE4443/14-1, BE4443/6-1, KFO309 P7 and SFB CRC1213-projects A02 and A04</funding_grant_id><funding_grant_id>Clinical career grant</funding_grant_id><pubmed_authors>Wu J</pubmed_authors><pubmed_authors>Barreto G</pubmed_authors><pubmed_authors>Bellusci S</pubmed_authors><pubmed_authors>Sedighi J</pubmed_authors><pubmed_authors>Chong L</pubmed_authors><pubmed_authors>Kolck J</pubmed_authors><pubmed_authors>Minoo P</pubmed_authors><pubmed_authors>Moiseenko A</pubmed_authors><pubmed_authors>Rako ZA</pubmed_authors><pubmed_authors>Carraro G</pubmed_authors><pubmed_authors>Warburton D</pubmed_authors><pubmed_authors>Young BM</pubmed_authors><pubmed_authors>Chao CM</pubmed_authors><pubmed_authors>Contreras A</pubmed_authors><pubmed_authors>Zimmermann V</pubmed_authors><pubmed_authors>Wilhelm J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Failure to Down-Regulate &lt;i>miR-154&lt;/i> Expression in Early Postnatal Mouse Lung Epithelium Suppresses Alveologenesis, with Changes in Tgf-β Signaling Similar to those Induced by Exposure to Hyperoxia.</name><description>&lt;h4>Background&lt;/h4>Bronchopulmonary dysplasia (BPD) is a lung disease of preterm born infants, characterized by alveolar simplification. MicroRNA (&lt;i>miR)&lt;/i> are known to be involved in many biological and pathological processes in the lung. Although a changed expression has been described for several &lt;i>miR&lt;/i> in BPD, a causal role remains to be established.&lt;h4>Results&lt;/h4>Our results showed that the expression level of &lt;i>miR-154&lt;/i> increases during lung development and decreases postnatally. Further, hyperoxia treatment maintains high levels of &lt;i>miR-154&lt;/i> in alveolar type 2 cells (AT2). We hypothesized that the decrease in &lt;i>miR-154&lt;/i> expression in AT2 cells is required for normal alveologenesis. To test this hypothesis, we generated a novel transgenic mouse allowing doxycycli</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Apr</publication><modification>2026-04-17T15:24:07.67Z</modification><creation>2020-05-23T07:09:43Z</creation></dates><accession>S-EPMC7226730</accession><cross_references><pubmed>32252341</pubmed><doi>10.3390/cells9040859</doi></cross_references></HashMap>