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dc.contributor.advisorTrojanowska, Mariaen_US
dc.contributor.advisorKim, Jiyounen_US
dc.contributor.authorMarden, Graceen_US
dc.date.accessioned2020-07-14T14:10:57Z
dc.date.available2020-07-14T14:10:57Z
dc.date.issued2020
dc.identifier.urihttps://hdl.handle.net/2144/41292
dc.description.abstractScleroderma (SSc) is an autoimmune disease characterized by dysfunctional immunity, vasculopathy, and fibrosis of the skin and internal organs. There is a poor prognosis for SSc patients and effective therapeutics have not yet been developed. Many mouse models have been developed, but most fail to recapitulate all of the symptoms seen in SSc patients. In this study we characterize a Fli1flox/flox mouse with CAG Cre under the beta-actin promoter. Based on what has been previously described in mice with deletion of Fli1 in specific cell types, we predicted that global postnatal deletion of Fli1 will result in systemic fibrosis, vasculopathy, and inflammation in these mice. The penetrance of a phenotype was highly variable; however, mice that developed a phenotype displayed disorganized vascular networks, fibrosis and proinflammatory cytokines and chemokines in the skin and lungs after 4 and 8 weeks of Fli1 deficiency. Increased macrophage and dendritic cell populations were observed in the lungs after 8 weeks. Fli1flox/flox CAG Cre mice exhibited hair loss after 5 months of Fli1 deletion. Since our experiments focus mainly on the lungs and skin, more experiments are required to characterize these mice to determine if they can be used as a novel animal model of SSc.en_US
dc.language.isoen_US
dc.subjectPathologyen_US
dc.subjectCAG Creen_US
dc.subjectFibrosisen_US
dc.subjectFli1en_US
dc.subjectMiceen_US
dc.subjectSystemic sclerosisen_US
dc.titleInvestigating the defects of postnatal global Fli1 deletion in a mouse modelen_US
dc.typeThesis/Dissertationen_US
dc.date.updated2020-07-13T22:03:11Z
etd.degree.nameMaster of Scienceen_US
etd.degree.levelmastersen_US
etd.degree.disciplinePathologyen_US
etd.degree.grantorBoston Universityen_US
dc.identifier.orcid0000-0001-7782-5420


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