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Title: Electrical signalling controls the mobility behaviour of osteoblast cells
Author: Chen, M.
Awarding Body: University of Aberdeen
Current Institution: University of Aberdeen
Date of Award: 2007
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Direct current (DC) electric fields (EF) as a guidance cue to influence the migration behaviours of osteoblasts were studied in detail for the first time. Direct current electric fields induced human primary osteoblast cells to migrate towards the anode and the osteoblast -like cell line TE85 migrated towards the cathode. In an EF, TE85 cells re-orientated and the long axis of cells were perpendicular to the vector of the electric field. This reorienting response showed voltage-dependence and could be blocked by the MAPK inhibitor U0126. Both growth factor bFGF and VEGF played an important role in the observed EF-induced migration. bFGF increased the migration speed and the directedness of migration in a physiological EF at a certain concentration of bFGF (l0ng/ml). VEGF increased the migration speed but reduced cathodal directedness. Immunofluorescence staining and quantitative confocal microscopy analysis showed that directed migration and perpendicular orientation of the TE85 cells were associated with the re-arrangement of F-actin filaments. U0126 blocked cell orientation in an EF with the disassembly of F-actin filaments. Electric fields failed to redistribute FGF receptors (FGFR) and bFGF in cells. MAPK signal transduction pathways were involved in the EF-induced cell migrations and Western blot revealed that EFs can increase the expression of active ERK1/2 but not of total ERKl/2. Further experiments focused on the effects of an applied EF on the murine preosteoblast cell line MC3T3. MC3T3 cells migrated towards cathode. In addition the applied EF increased the expression of the early osteogenic marker collagen I and reduced the expression of alkaline phosphatase and osteocalcin, with no change of osteopontin and runx-2. These novel findings on osteoblast cell responses to a physiological EF could lead to new insights into the concept of bone development and new clinical treatment for bone repair.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available