{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Unachukwu U"],"funding":["NHLBI NIH HHS","NIGMS NIH HHS"],"pagination":["2340-2351"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6191095"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["31(6)"],"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<sup>3</sup>) or room air, and offspring were humanely killed on 12.5, 14.5, 16.5, and 18.5 d <i>post coitum</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"],"journal":["FASEB journal : official publication of the Federation of American Societies for Experimental Biology"],"pubmed_title":["Maternal smoke exposure decreases mesenchymal proliferation and modulates Rho-GTPase-dependent actin cytoskeletal signaling in fetal lungs."],"pmcid":["PMC6191095"],"funding_grant_id":["R01 HL086936","T32 GM008464"],"pubmed_authors":["Trischler J","Goldklang M","D'Armiento J","Unachukwu U","Xiao R"],"additional_accession":[]},"is_claimable":false,"name":"Maternal smoke exposure decreases mesenchymal proliferation and modulates Rho-GTPase-dependent actin cytoskeletal signaling in fetal lungs.","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<sup>3</sup>) or room air, and offspring were humanely killed on 12.5, 14.5, 16.5, and 18.5 d <i>post coitum</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","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Jun","modification":"2025-04-18T23:54:15.98Z","creation":"2019-03-27T00:03:14Z"},"accession":"S-EPMC6191095","cross_references":{"pubmed":["28209772"],"doi":["10.1096/fj.201601063R","10.1096/fj.201601063r"]}}