ingest cdrApp 2018-06-13T15:17:54.257Z 51cd2fe2-3fd7-401f-a923-a97bc3db68a2 modifyDatastreamByValue RELS-EXT fedoraAdmin 2018-06-13T15:44:19.193Z Setting exclusive relation addDatastream MD_TECHNICAL fedoraAdmin 2018-06-13T15:44:30.821Z Adding technical metadata derived by FITS addDatastream MD_FULL_TEXT fedoraAdmin 2018-06-13T15:44:53.443Z Adding full text metadata extracted by Apache Tika modifyDatastreamByValue RELS-EXT fedoraAdmin 2018-06-13T15:44:54.128Z Setting exclusive relation modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2018-07-16T21:30:00.884Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2018-08-22T15:46:32.765Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2018-09-28T18:34:04.693Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2018-10-12T17:24:29.720Z modifyDatastreamByValue MD_DESCRIPTIVE cdrApp 2019-03-22T20:46:17.583Z Yina Li Author Department of Orthodontics School of Dentistry THE ROLE OF AUTOPHAGY DURING ORTHODONTIC TOOTH MOVEMENT Orthodontic tooth movement (OTM) depends on efficient remodeling of surrounding alveolar bone. While a well-controlled inflammatory response is essential during such biological processes, the precise mechanism by which how inflammation is regulated hasn’t been fully understood. Autophagy, a conserved catabolic pathway, has been shown to protect cells from excessive long lasting inflammation in nervous systems and other disease conditions. We hypothesize that autophagy plays a role in regulating inflammation during OTM. By using a split mouth design in adult male mice at different time points (days 0, 1, 3, 5, 7, 10 and 14) after 30 gram of force loading, we found that autophagy activity increased shortly after loading (as early as day 1) and was closely associated with inflammatory cytokine expression as well as osteoclast activation (by TRAP staining). Autophagy activation appeared to be at the protein, not mRNA, level. Daily administration of rapamycin, autophagy activator, in adult male mice led to reduced tooth movement amount as well as inflammatory signal after loading, suggesting a negative effect of autophagy on inflammatory response during OTM. To our knowledge, this is the first time that research showed autophagy plays a role during orthodontic tooth movement, likely via negative regulation of inflammatory response. More molecular and cellular analyses are needed to elucidate the underlying mechanism that governs the regulation of inflammation by autophagy pathway. Spring 2018 2018 Biology autophagy, inflammation, orthodontic, tooth movement eng Master of Science Thesis University of North Carolina at Chapel Hill Graduate School Degree granting institution Dentistry (Orthodontics) Ching-Chang Ko Thesis advisor Jennifer Martinez Thesis advisor Henry Tseng Thesis advisor text Yina Li Author Department of Orthodontics School of Dentistry THE ROLE OF AUTOPHAGY DURING ORTHODONTIC TOOTH MOVEMENT Orthodontic tooth movement (OTM) depends on efficient remodeling of surrounding alveolar bone. While a well-controlled inflammatory response is essential during such biological processes, the precise mechanism by which how inflammation is regulated hasn’t been fully understood. Autophagy, a conserved catabolic pathway, has been shown to protect cells from excessive long lasting inflammation in nervous systems and other disease conditions. We hypothesize that autophagy plays a role in regulating inflammation during OTM. By using a split mouth design in adult male mice at different time points (days 0, 1, 3, 5, 7, 10 and 14) after 30 gram of force loading, we found that autophagy activity increased shortly after loading (as early as day 1) and was closely associated with inflammatory cytokine expression as well as osteoclast activation (by TRAP staining). Autophagy activation appeared to be at the protein, not mRNA, level. Daily administration of rapamycin, autophagy activator, in adult male mice led to reduced tooth movement amount as well as inflammatory signal after loading, suggesting a negative effect of autophagy on inflammatory response during OTM. To our knowledge, this is the first time that research showed autophagy plays a role during orthodontic tooth movement, likely via negative regulation of inflammatory response. More molecular and cellular analyses are needed to elucidate the underlying mechanism that governs the regulation of inflammation by autophagy pathway. Spring 2018 2018 Biology autophagy, inflammation, orthodontic, tooth movement eng Master of Science Thesis University of North Carolina at Chapel Hill Graduate School Degree granting institution Dentistry (Orthodontics) Ching-Chang Ko Thesis advisor Jennifer Martinez Thesis advisor Henry Tseng Thesis advisor text Yina Li Author Department of Orthodontics School of Dentistry THE ROLE OF AUTOPHAGY DURING ORTHODONTIC TOOTH MOVEMENT Orthodontic tooth movement (OTM) depends on efficient remodeling of surrounding alveolar bone. While a well-controlled inflammatory response is essential during such biological processes, the precise mechanism by which how inflammation is regulated hasn’t been fully understood. Autophagy, a conserved catabolic pathway, has been shown to protect cells from excessive long lasting inflammation in nervous systems and other disease conditions. We hypothesize that autophagy plays a role in regulating inflammation during OTM. By using a split mouth design in adult male mice at different time points (days 0, 1, 3, 5, 7, 10 and 14) after 30 gram of force loading, we found that autophagy activity increased shortly after loading (as early as day 1) and was closely associated with inflammatory cytokine expression as well as osteoclast activation (by TRAP staining). Autophagy activation appeared to be at the protein, not mRNA, level. Daily administration of rapamycin, autophagy activator, in adult male mice led to reduced tooth movement amount as well as inflammatory signal after loading, suggesting a negative effect of autophagy on inflammatory response during OTM. To our knowledge, this is the first time that research showed autophagy plays a role during orthodontic tooth movement, likely via negative regulation of inflammatory response. More molecular and cellular analyses are needed to elucidate the underlying mechanism that governs the regulation of inflammation by autophagy pathway. Spring 2018 2018 Biology autophagy, inflammation, orthodontic, tooth movement eng Master of Science Thesis Dentistry (Orthodontics) Ching-Chang Ko Thesis advisor Jennifer Martinez Thesis advisor Henry Tseng Thesis advisor text University of North Carolina at Chapel Hill Degree granting institution Yina Li Creator Department of Orthodontics School of Dentistry THE ROLE OF AUTOPHAGY DURING ORTHODONTIC TOOTH MOVEMENT Orthodontic tooth movement (OTM) depends on efficient remodeling of surrounding alveolar bone. While a well-controlled inflammatory response is essential during such biological processes, the precise mechanism by which how inflammation is regulated hasn’t been fully understood. Autophagy, a conserved catabolic pathway, has been shown to protect cells from excessive long lasting inflammation in nervous systems and other disease conditions. We hypothesize that autophagy plays a role in regulating inflammation during OTM. By using a split mouth design in adult male mice at different time points (days 0, 1, 3, 5, 7, 10 and 14) after 30 gram of force loading, we found that autophagy activity increased shortly after loading (as early as day 1) and was closely associated with inflammatory cytokine expression as well as osteoclast activation (by TRAP staining). Autophagy activation appeared to be at the protein, not mRNA, level. Daily administration of rapamycin, autophagy activator, in adult male mice led to reduced tooth movement amount as well as inflammatory signal after loading, suggesting a negative effect of autophagy on inflammatory response during OTM. To our knowledge, this is the first time that research showed autophagy plays a role during orthodontic tooth movement, likely via negative regulation of inflammatory response. More molecular and cellular analyses are needed to elucidate the underlying mechanism that governs the regulation of inflammation by autophagy pathway. Biology autophagy; inflammation; orthodontic; tooth movement eng Master of Science Masters Thesis Dentistry (Orthodontics) Ching-Chang Ko Thesis advisor Jennifer Martinez Thesis advisor Henry Tseng Thesis advisor text University of North Carolina at Chapel Hill Degree granting institution 2018 2018-05 Yina Li Author Department of Orthodontics School of Dentistry THE ROLE OF AUTOPHAGY DURING ORTHODONTIC TOOTH MOVEMENT Orthodontic tooth movement (OTM) depends on efficient remodeling of surrounding alveolar bone. While a well-controlled inflammatory response is essential during such biological processes, the precise mechanism by which how inflammation is regulated hasn’t been fully understood. Autophagy, a conserved catabolic pathway, has been shown to protect cells from excessive long lasting inflammation in nervous systems and other disease conditions. We hypothesize that autophagy plays a role in regulating inflammation during OTM. By using a split mouth design in adult male mice at different time points (days 0, 1, 3, 5, 7, 10 and 14) after 30 gram of force loading, we found that autophagy activity increased shortly after loading (as early as day 1) and was closely associated with inflammatory cytokine expression as well as osteoclast activation (by TRAP staining). Autophagy activation appeared to be at the protein, not mRNA, level. Daily administration of rapamycin, autophagy activator, in adult male mice led to reduced tooth movement amount as well as inflammatory signal after loading, suggesting a negative effect of autophagy on inflammatory response during OTM. To our knowledge, this is the first time that research showed autophagy plays a role during orthodontic tooth movement, likely via negative regulation of inflammatory response. More molecular and cellular analyses are needed to elucidate the underlying mechanism that governs the regulation of inflammation by autophagy pathway. Spring 2018 2018 Biology autophagy, inflammation, orthodontic, tooth movement eng Master of Science Thesis University of North Carolina at Chapel Hill Graduate School Degree granting institution Dentistry (Orthodontics) Ching-Chang Ko Thesis advisor Jennifer Martinez Thesis advisor Henry Tseng Thesis advisor text Yina Li Creator Department of Orthodontics School of Dentistry Orthodontic tooth movement (OTM) depends on efficient remodeling of surrounding alveolar bone. While a well-controlled inflammatory response is essential during such biological processes, the precise mechanism by which how inflammation is regulated hasn’t been fully understood. Autophagy, a conserved catabolic pathway, has been shown to protect cells from excessive long lasting inflammation in nervous systems and other disease conditions. We hypothesize that autophagy plays a role in regulating inflammation during OTM. By using a split mouth design in adult male mice at different time points (days 0, 1, 3, 5, 7, 10 and 14) after 30 gram of force loading, we found that autophagy activity increased shortly after loading (as early as day 1) and was closely associated with inflammatory cytokine expression as well as osteoclast activation (by TRAP staining). Autophagy activation appeared to be at the protein, not mRNA, level. Daily administration of rapamycin, autophagy activator, in adult male mice led to reduced tooth movement amount as well as inflammatory signal after loading, suggesting a negative effect of autophagy on inflammatory response during OTM. To our knowledge, this is the first time that research showed autophagy plays a role during orthodontic tooth movement, likely via negative regulation of inflammatory response. More molecular and cellular analyses are needed to elucidate the underlying mechanism that governs the regulation of inflammation by autophagy pathway. 2018-05 2018 Biology autophagy; inflammation; orthodontic; tooth movement eng Master of Science Masters Thesis University of North Carolina at Chapel Hill Graduate School Degree granting institution Ching-Chang Ko Thesis advisor Jennifer Martinez Thesis advisor Henry Tseng Thesis advisor text Li_unc_0153M_17570.pdf uuid:50d5c878-7463-4c36-be06-e3c203defa45 2020-06-13T00:00:00 2018-03-30T14:56:16Z proquest application/pdf 7498149