title: Maternal hepatic growth response to pregnancy in the mouse.
abstract: Pregnancy is characterized by physiological adjustments in the maternal compartment. In this investigation, the influence of pregnancy on maternal liver was examined in CD-1 mice. Dramatic changes were observed in the size of the maternal liver during pregnancy. Livers doubled in weight from the non-pregnant state to day 18 of pregnancy. The pregnancy-induced hepatomegaly was a physiological event of liver growth confirmed by DNA content increase and detection of hepatocyte hyperplasia and hypertrophy. Growth of the liver was initiated following implantation and peaked at parturition. The expression and/or activities of key genes known to regulate liver regeneration, a phenomenon of liver growth compensatory to liver mass loss, were investigated. The results showed that pregnancy-dependent liver growth was associated with interleukin (IL)-6, tumor necrosis factor α, c-Jun and IL-1β, but independent of hepatocyte growth factor, fibroblast growth factor 1, tumor necrosis factor receptor 1, constitutive androstane receptor and pregnane X receptor. Furthermore, maternal liver growth was associated with the activation of hepatic signal transducer and activator of transcription 3, β-catenin and epidermal growth factor receptor, but pregnancy did not activate hepatic c-Met. The findings suggest that the molecular mechanisms regulating pregnancy-induced liver growth and injury-induced liver regeneration exhibit overlapping features but are not identical. In summary, the liver of the mouse adapts to the demands of pregnancy via a dramatic growth response driven by hepatocyte proliferation and size increase.
authors.affiliation: Department of Biology, Center for Regenerative Biology and Medicine, School of Science, Indiana University-Purdue University Indianapolis, Indianapolis, IN 46202, USA.
authors.forename: Guoli
authors.initials: G
authors.lastname: Dai
authors.forename: Juan J
authors.initials: JJ
authors.lastname: Bustamante
authors.forename: Yuhong
authors.initials: Y
authors.lastname: Zou
authors.forename: Andriy
authors.initials: A
authors.lastname: Myronovych
authors.forename: Qi
authors.initials: Q
authors.lastname: Bao
authors.forename: Sudhanshu
authors.initials: S
authors.lastname: Kumar
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Soares
mesh_terms: D000818:Animals; D000090702:Constitutive Androstane Receptor; D010064:Embryo Implantation / Q000502:physiology; D066246:ErbB Receptors / Q000378:metabolism; D005260:Female; D016220:Fibroblast Growth Factor 1 / Q000378:metabolism; D017228:Hepatocyte Growth Factor / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008099:Liver / Q000033:anatomy & histology* / Q000254:growth & development; D051379:Mice; D036801:Parturition / Q000502:physiology; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000502:physiology*; D000077297:Pregnane X Receptor; D016755:Proto-Oncogene Proteins c-jun / Q000378:metabolism; D019859:Proto-Oncogene Proteins c-met / Q000378:metabolism; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism; D011987:Receptors, Steroid / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism; D050796:STAT3 Transcription Factor / Q000378:metabolism; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D051176:beta Catenin / Q000378:metabolism
chemical_list: D000090702:Constitutive Androstane Receptor; D053583:Interleukin-1beta; D015850:Interleukin-6; D000077297:Pregnane X Receptor; D016755:Proto-Oncogene Proteins c-jun; D018160:Receptors, Cytoplasmic and Nuclear; D011987:Receptors, Steroid; D018124:Receptors, Tumor Necrosis Factor; D050796:STAT3 Transcription Factor; C494087:Stat3 protein, mouse; D014409:Tumor Necrosis Factor-alpha; D051176:beta Catenin; D016220:Fibroblast Growth Factor 1; D017228:Hepatocyte Growth Factor; D066246:ErbB Receptors; D019859:Proto-Oncogene Proteins c-met