title: Decidual cell polyploidization necessitates mitochondrial activity.
abstract: Cellular polyploidy has been widely reported in nature, yet its developmental mechanism and function remain poorly understood. In the present study, to better define the aspects of decidual cell polyploidy, we isolated pure polyploid and non-polyploid decidual cell populations from the in vivo decidual bed. Three independent RNA pools prepared for each population were then subjected to the Affymetrix gene chip analysis for the whole mouse genome transcripts. Our data revealed up-regulation of 1015 genes and down-regulation of 1207 genes in the polyploid populations, as compared to the non-polyploid group. Comparative RT-PCR and in situ hybridization results indeed confirmed differential expressional regulation of several genes between the two populations. Based on functional enrichment analyses, up-regulated polyploidy genes appeared to implicate several functions, which primarily include cell/nuclear division, ATP binding, metabolic process, and mitochondrial activity, whereas that of down-regulated genes primarily included apoptosis and immune processes. Further analyses of genes that are related to mitochondria and bi-nucleation showed differential and regional expression within the decidual bed, consistent with the pattern of polyploidy. Consistently, studies revealed a marked induction of mitochondrial mass and ATP production in polyploid cells. The inhibition of mitochondrial activity by various pharmacological inhibitors, as well as by gene-specific targeting using siRNA-mediated technology showed a dramatic attenuation of polyploidy and bi-nucleation development during in vitro stromal cell decidualization, suggesting mitochondria play a major role in positive regulation of decidual cell polyploidization. Collectively, analyses of unique polyploidy markers and molecular signaling networks may be useful to further characterize functional aspects of decidual cell polyploidy at the site of implantation.
authors: Division of Reproductive Sciences, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States of America.
authors: Xinghong
authors: X
authors: Ma
authors: Fei
authors: F
authors: Gao
authors: Allison
authors: A
authors: Rusie
authors: Jennifer
authors: J
authors: Hemingway
authors: Alicia B
authors: AB
authors: Ostmann
authors: Julie M
authors: JM
authors: Sroga
authors: Anil G
authors: AG
authors: Jegga
authors: Sanjoy K
authors: SK
authors: Das
mesh_terms: D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000818:Animals; D017209:Apoptosis / Q000235:genetics; D002455:Cell Division / Q000235:genetics; D003656:Decidua / Q000166:cytology*; D005260:Female; D005786:Gene Expression Regulation; D051379:Mice; D008928:Mitochondria / Q000378:metabolism* / Q000502:physiology; D011123:Polyploidy; D059467:Transcriptome
chemical_list: D000255:Adenosine Triphosphate