<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Unachukwu U</submitter><funding>NHLBI NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>2340-2351</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6191095</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>31(6)</volume><pubmed_abstract>The present study tested the hypothesis that maternal smoke exposure results in fetal lung growth retardation due to dysregulation in various signaling pathways, including the Wnt (wingless-related integration site)/β-catenin pathway. Pregnant female C57BL/6J mice were exposed to cigarette smoke (100-150 mg/m&lt;sup>3&lt;/sup>) or room air, and offspring were humanely killed on 12.5, 14.5, 16.5, and 18.5 d &lt;i>post coitum&lt;/i> (dpc). We assessed lung stereology with Cavalieri estimation; apoptosis with proliferating cell nuclear antigen, TUNEL, and caspase assays; and gene expression with quantitative PCR (qPCR) and RNA sequencing on lung epithelium and mesenchyme retrieved by laser capture microdissection. Results demonstrated a significant decrease in body weight and lung volume of smoke-exposed</pubmed_abstract><journal>FASEB journal : official publication of the Federation of American Societies for Experimental Biology</journal><pubmed_title>Maternal smoke exposure decreases mesenchymal proliferation and modulates Rho-GTPase-dependent actin cytoskeletal signaling in fetal lungs.</pubmed_title><pmcid>PMC6191095</pmcid><funding_grant_id>R01 HL086936</funding_grant_id><funding_grant_id>T32 GM008464</funding_grant_id><pubmed_authors>Trischler J</pubmed_authors><pubmed_authors>Goldklang M</pubmed_authors><pubmed_authors>D'Armiento J</pubmed_authors><pubmed_authors>Unachukwu U</pubmed_authors><pubmed_authors>Xiao R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Maternal smoke exposure decreases mesenchymal proliferation and modulates Rho-GTPase-dependent actin cytoskeletal signaling in fetal lungs.</name><description>The present study tested the hypothesis that maternal smoke exposure results in fetal lung growth retardation due to dysregulation in various signaling pathways, including the Wnt (wingless-related integration site)/β-catenin pathway. Pregnant female C57BL/6J mice were exposed to cigarette smoke (100-150 mg/m&lt;sup>3&lt;/sup>) or room air, and offspring were humanely killed on 12.5, 14.5, 16.5, and 18.5 d &lt;i>post coitum&lt;/i> (dpc). We assessed lung stereology with Cavalieri estimation; apoptosis with proliferating cell nuclear antigen, TUNEL, and caspase assays; and gene expression with quantitative PCR (qPCR) and RNA sequencing on lung epithelium and mesenchyme retrieved by laser capture microdissection. Results demonstrated a significant decrease in body weight and lung volume of smoke-exposed</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Jun</publication><modification>2025-04-18T23:54:15.98Z</modification><creation>2019-03-27T00:03:14Z</creation></dates><accession>S-EPMC6191095</accession><cross_references><pubmed>28209772</pubmed><doi>10.1096/fj.201601063R</doi><doi>10.1096/fj.201601063r</doi></cross_references></HashMap>