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dc.contributor.advisorAkçalı, K. Canen_US
dc.contributor.authorAyaloğlu Bütün, Fatmaen_US
dc.date.accessioned2016-01-08T18:24:11Z
dc.date.available2016-01-08T18:24:11Z
dc.date.issued2011
dc.identifier.urihttp://hdl.handle.net/11693/15756
dc.descriptionAnkara : The Department of Molecular Biology and Genetics and the Graduate School of Engineering and Science of Bilkent University, 2011.en_US
dc.descriptionThesis (Ph. D.) -- Bilkent University, 2011.en_US
dc.descriptionIncludes bibliographical references leaves 104-122.en_US
dc.description.abstractMesenchymal Stem Cells (MSCs) can self renew and differentiate into different cell types like, adipocytes, osteoblasts, chondrocytes, neurons, hepatocytes and endothelial cells. Their ability to differentiate into wide variety of cell types, nonimmunogenic characteristics, along with homing capacity to injured tissue and the absence of any ethical issue related to their uses, make MSCs important in regenerative medicine and tissue engineering. Their ability to migrate to the site of injury raises the opportunity of these stem cells to be considered also as in vivo delivery agents. However, one major obstacle in using MSCs in cell based therapies is their limited numbers. Estrogen is known to have role in growth, proliferation and apoptosis. Therefore our aim was to study the possible role and mechanism of estrogen in their maintenance and their homing capacity. We used MSCs derived from female and ovariectomized female rat bone marrow in our research. Our results revealed that estrogen treatment increased the number of colonies and the number of cells constituting a colony. Estrogen decreased the differentiation capacity of MSCs to the adipogenic lineages as shown by reduced of Oil Red O staining Estrogen also affected MSCs’ homing capacity. Estrogen treatment resulted in the migration of increased number of DiI labeled MSCs to the site of injury after partial hepatectomy (PH) compared to that of untreated MSCs. Furthermore, estrogen treatment decreased the rate of apoptosis. Our data showed that estrogen regulates apoptosis through Bcl-2 family of genes in MSCs. This regulation was at the protein level but not at the transcript level. Estrogen addition increased the expression of anti-apoptotic members of the Bcl-2 family of proteins, Bcl-2 and Bcl-xL. The decrease in the apoptosis was not observed when Bcl-xL and Bcl-2 genes were knocked down. The silencing histone code H3K27me3 was also decreased in estrogen treated MSCs, suggesting an epigenetic regulation of MSCs upon estrogen treatment. Altogether our results show that estrogen increased the number of functional MSCs, decreased spontaneous apoptosis in these cells, and improved the homing capacity of rat bone marrow derived MSCs. Therefore, estrogen treatment of MSCs may offer new opportunities for the therapeutic actions of these cells.en_US
dc.description.statementofresponsibilityBütün, Fatma Ayaloğluen_US
dc.format.extentxvii, 130 leaves, illustrationsen_US
dc.language.isoEnglishen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subject.lccQH588.S83 B88 2011en_US
dc.subject.lcshMesenchymal stem cells.en_US
dc.subject.lcshStem cells.en_US
dc.subject.lcshHormone therapy.en_US
dc.subject.lcshEstrogen replacement therapy.en_US
dc.titleRole of estrogen on the maintenance and homing capacity of bone marrow derived rat mesenchymal stem cellsen_US
dc.typeThesisen_US
dc.departmentDepartment of Molecular Biology and Geneticsen_US
dc.publisherBilkent Universityen_US
dc.description.degreePh.D.en_US


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