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dc.contributor.supervisor Keijzer, Richard (Surgery) en_US
dc.contributor.author Visser, Robin
dc.date.accessioned 2016-01-14T15:01:33Z
dc.date.available 2016-01-14T15:01:33Z
dc.date.issued 2015
dc.identifier.uri http://hdl.handle.net/1993/31060
dc.description.abstract INTRODUCTION: Pulmonary hypoplasia causes high morbidity and mortality in congenital diaphragmatic hernia (CDH) patients. MiR-10a and miR-200b are overexpressed in human CDH lungs. We aimed to define their roles in lung development. METHODS: We profiled miR-10a expression with RT-qPCR and in situ hybridization using a nitrofen rat model for CDH. The effects of miR-10a on airway branching were evaluated in lung explants. MiR-200b’s role in airway branching was assessed in miR-200b knockout lung explants. Crossing miR-200b knockout mice with CFP-E-Cadherin was used to evaluate miR-200b’s effects on epithelial differentiation. RESULTS: Expression of miR-10a was altered in the nitrofen model and miR-10a mimics reversed lung hypoplasia in vitro. Heterozygous miR-200b lung explants displayed reduced airway branching. CFP-E-Cadherin/miR-200b knockout lung explants showed reduced epithelial expression. CONCLUSION: Both miR-10a and miR-200b are critical for lung development and CDH. Normalizing their expression may reverse lung hypoplasia and reduce the associated morbidity and mortality in CDH. en_US
dc.rights info:eu-repo/semantics/openAccess
dc.subject congenital diaphragmatic hernia en_US
dc.subject lung development en_US
dc.subject miR-10a en_US
dc.subject miR-200b en_US
dc.subject pulmonary hypoplasia en_US
dc.title MiRacles for babies with pulmonary hypoplasia: the effects of miR-10a and miR-200b on lung development en_US
dc.type info:eu-repo/semantics/masterThesis
dc.degree.discipline Surgery en_US
dc.contributor.examiningcommittee Boyd, April (Surgery) Pathak, Alok (Surgery) Ghavami, Saied (Human Anatomy and Cell Science) en_US
dc.degree.level Master of Science (M.Sc.) en_US
dc.description.note February 2016 en_US


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