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dc.contributor.authorDudley, Elizabeth Ann
dc.date.accessioned2016-04-29T04:30:18Z
dc.date.available2016-04-29T04:30:18Z
dc.date.issued2015-12
dc.identifier.otherdudley_elizabeth_a_201512_ms
dc.identifier.urihttp://purl.galileo.usg.edu/uga_etd/dudley_elizabeth_a_201512_ms
dc.identifier.urihttp://hdl.handle.net/10724/35182
dc.description.abstractLysophosphatidic acid (LPA) is a signaling molecule that acts through six G-protein coupled receptors, LPA1-6. LPA3-deficiency in mice was previously shown to cause delayed implantation, embryo crowding, and placental hypertrophy that were only associated with maternal genotype and not fetal genotypes. It was hypothesized that Lpar3-deficiency alters placentation which may lead to placental hypertrophy. Realtime PCR, for temporal expression of Lpar3 in placenta; in situ hybridization, for localization of Lpar3 in D13.5 placenta; and histology of D13.5 placentas were conducted. These data demonstrated spatiotemporal expression of Lpar3 mRNA in the mouse placenta and a critical role of maternal LPA3 in the mouse placental development. Additionally, it was hypothesized that LPA3-mediated signaling may promote uterine stromal cell proliferation to prepare the uterus for embryo implantation via ERK phosphorylation. Preliminary data indicate that the total ERK is not altered in the preimplantation D3.5 Lpar3-deficient uterus.
dc.languageeng
dc.publisheruga
dc.rightsOn Campus Only Until 2017-12-01
dc.subjectLPA
dc.subjectLPA3
dc.subjectLpar3-/- mice
dc.subjectplacenta
dc.subjectuterus
dc.subjectERK
dc.titleRole of LPA3 in mouse placental development
dc.typeThesis
dc.description.degreeMS
dc.description.departmentPhysiology and Pharmacology
dc.description.majorToxicology
dc.description.advisorXiaoqin Ye
dc.description.committeeXiaoqin Ye
dc.description.committeeMary Alice Smith
dc.description.committeeShelley Hooks


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