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dc.contributor.authorCheng, Thomas Wen-Taoen_US
dc.date.accessioned2016-05-13T14:42:26Z
dc.date.available2016-05-13T14:42:26Z
dc.date.issued2015
dc.identifier.urihttps://hdl.handle.net/2144/16261
dc.description.abstractBone is one of the few organs capable of regeneration after a substantial injury. As the bone heals itself after trauma, the coupling of angiogenesis to osteogenesis is crucial for the restoration of the skeletal tissue. In prior studies we have shown that Bone Morphogenetic Protein 2 (BMP2), a potent agonist for skeletal formation is expressed by vessels making it a prime candidate that links the morphogenesis of the two tissues. To investigate the role of BMP2 in the coordination of vessel and bone formation, we used a tamoxifen inducible Smooth Muscle Actin (SMA) promoter that conditionally expresses Cre recombinases crossed with a BMP2 floxed mouse in order to conditionally delete the BMP2 gene in smooth muscle actin (SMA) expressing cells. Using the mouse femur as our model for bone regeneration, we performed a surgical technique called distraction osteogenesis (DO) where an osteotomy is created followed by distraction or a gradual separation of the two pieces of bone. This primarily promotes intramembranous ossification at the osteotomy site by mechanical stimulation. Tamoxifen treatment started at day 6 and continued throughout the experiment. At post-operative days 3, 7, 12, 17, 24, and 31, we analyzed the bone and vessel formation by plain X-ray, micro-computed tomography (µCT) and vascular contrast enhanced µCT, and quantitative polymerase chain reaction (qPCR) of selective genes. We assessed both the femur and surrounding tissue to obtain qualitative and quantitative assessments for skeletal and vascular formation. Our results demonstrated that the deletion of BMP2 in vascular tissue resulted in a reduction of angiogenesis in vivo followed by a decrease in skeletal tissue development.en_US
dc.language.isoen_US
dc.rightsAttribution 4.0 Internationalen_US
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectMedicineen_US
dc.subjectAngiogenesisen_US
dc.subjectBone morphogenetic protein 2en_US
dc.subjectOsteogenesisen_US
dc.subjectSMAen_US
dc.subjectBone repairen_US
dc.subjectDistraction osteogenesisen_US
dc.titleThe role of bone morphogenetic protein 2 in SMA-directed angiogenesis during distraction osteogenesisen_US
dc.typeThesis/Dissertationen_US
dc.date.updated2016-04-08T20:20:06Z
etd.degree.nameMaster of Scienceen_US
etd.degree.levelmastersen_US
etd.degree.disciplineMedical Sciencesen_US
etd.degree.grantorBoston Universityen_US


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Attribution 4.0 International
Except where otherwise noted, this item's license is described as Attribution 4.0 International