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Influence of murine maternal diabetes on placental morphology, gene expression, and function
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Physiology and Developmental Biology, Animal Development and Genetics.
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Physiology and Developmental Biology, Animal Development and Genetics.
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Physiology and Developmental Biology, Animal Development and Genetics.
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2008 (English)In: Archives of Physiology and Biochemistry, ISSN 1381-3455, E-ISSN 1744-4160, Vol. 114, no 2, 99-110 p.Article in journal (Refereed) Published
Place, publisher, year, edition, pages
2008. Vol. 114, no 2, 99-110 p.
National Category
Developmental Biology
Identifiers
URN: urn:nbn:se:uu:diva-96496DOI: 10.1080/13813450802033776OAI: oai:DiVA.org:uu-96496DiVA: diva2:171091
Available from: 2007-11-21 Created: 2007-11-21 Last updated: 2017-12-14Bibliographically approved
In thesis
1. Molecular Mechanisms Underlying Abnormal Placentation in the Mouse
Open this publication in new window or tab >>Molecular Mechanisms Underlying Abnormal Placentation in the Mouse
2007 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Placental development can be disturbed by various factors, such as mutation of specific genes or maternal diabetes. Our previous work on interspecies hybrid placental dysplasia (IHPD) and two additional models of placental hyperplasia, cloned mice and Esx1 mutants, showed that many genes are deregulated in placental dysplasia. Two of these candidate placentation genes, Cpe and Lhx3, were further studied. We performed in situ hybridization to determine their spatio-temporal expression in the placentas and placental phenotypes were analyzed in mutant mice. Our results showed that the placental phenotype in Cpe mutant mice mimics some IHPD phenotypes. Deregulated expression of Cpe and Cpd, a functionally equivalent gene, prior to the manifestation of the IHPD phenotype, indicated that Cpe and Cpd are potentially causative genes in IHPD. Lhx3 mutants lacked any placental phenotype. Deletion of Lhx3 and Lhx4 together caused an inconsistent placental phenotype which did not affect placental lipid transport function or expression of Lhx3/Lhx4 target genes. Down regulation of Lhx3/Lhx4 did not rescue the placental phenotype of AT24 mice and hence could be excluded as causative genes in IHPD. Analysis of placental development in diabetic mice showed that severe maternal diabetes resulted in fetal intrauterine growth restriction (IUGR) without any change in placental weight and lipid transport function. The diabetic placentas however exhibited abnormal morphology. Gene expression profiling identified some genes that might contribute to diabetic pathology. In another study, it was found that the heterochromatin protein CBX1 is required for normal placentation, as deletion of the gene caused consistent spongiotrophoblast and labyrinthine phenotypes. Gene expression profiling and spatio-temporal expression analysis showed that several genes with known function in placental development were deregulated in the Cbx1 null placenta.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2007. 52 p.
Series
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Science and Technology, ISSN 1651-6214 ; 371
Keyword
Developmental biology, IUGR, Placental phenotype, Placental hyperplasia, Diabetes, IHPD, Utvecklingsbiologi
National Category
Developmental Biology
Identifiers
urn:nbn:se:uu:diva-8331 (URN)978-91-554-7037-1 (ISBN)
Public defence
2007-12-12, Lindahlsalen, EBC, 18A, Norbyvägen, Uppsala, 75236., 10:00 (English)
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Available from: 2007-11-21 Created: 2007-11-21 Last updated: 2010-02-04Bibliographically approved

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Fundele, Reinald H.

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