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This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 34/2/193    most recent 00220.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Rampon, C. Articles by Huber, P. PubMed PubMed Citation Articles by Rampon, C. Articles by Huber, P.

Protocadherin 12 deficiency alters morphogenesis and transcriptional profile of the placenta

¹ Laboratory of Vascular Pathophysiology, Institut National de la Santé et de la Recherche Médicale U882, Commissariat à l'Énergie Atomique (CEA), Grenoble University, CEA, Grenoble, France
² Laboratory of Informatics and Mathematics for Biology, CEA, Grenoble, France

Protocadherins are transmembrane proteins exhibiting homophilic adhesive activities through their extracellular domain. Protocadherin 12 (Pcdh12) is expressed in angiogenic endothelial cells, mesangial cells of kidney glomeruli, and glycogen cells of the mouse placenta. To get insight into the role of this protein in vivo, we analyzed PCDH12-deficient mice and investigated their placental phenotype. The mice were alive and fertile; however, placental and embryonic sizes were reduced compared with wild-type mice. We observed defects in placental layer segregation and a decreased vascularization of the labyrinth associated with a reduction in cell density in this layer. To understand the molecular events responsible for the phenotypic alterations observed in Pcdh12^–/– placentas, we analyzed the expression profile of embryonic day 12.5 mutant placentas compared with wild-type placentas, using pangenomic chips: 2,289 genes exhibited statistically significant changes in expressed levels due to loss of PCDH12. Functional grouping of modified genes was obtained by GoMiner software. Gene clusters that contained most of the differentially expressed genes were those involved in tissue morphogenesis and development, angiogenesis, cell-matrix adhesion and migration, immune response, and chromatin remodeling. Our data show that loss of PCDH12 leads to morphological alterations of the placenta and to notable changes in its gene expression profile. Specific genes emerging from the microarray screen support the biological modifications observed in PCDH12-deficient placentas.

knockout mice; gene profiling; trophoblasts; angiogenesis