@article{(Open Science Index):https://publications.waset.org/pdf/761,
	  title     = {Bone Generation through Mechanical Loading},
	  author    = {R. S. A. Nesbitt and  J. Macione and  A. Debroy and  S. P. Kotha},
	  country	= {},
	  institution	= {},
	  abstract     = {Bones are dynamic and responsive organs, they
regulate their strength and mass according to the loads which they are subjected. Because, the Wnt/β-catenin pathway has profound
effects on the regulation of bone mass, we hypothesized that mechanical loading of bone cells stimulates Wnt/β-catenin signaling, which results in the generation of new bone mass.
Mechanical loading triggers the secretion of the Wnt molecule, which after binding to transmembrane proteins, causes GSK-3β (Glycogen synthase kinase 3 beta) to cease the phosphorylation of β-catenin. β-catenin accumulation in the cytoplasm, followed by its
transport into the nucleus, binding to transcription factors (TCF/LEF)
that initiate transcription of genes related to bone formation. To test this hypothesis, we used TOPGAL (Tcf Optimal Promoter
β-galactosidase) mice in an experiment in which cyclic loads were
applied to the forearm. TOPGAL mice are reporters for cells effected
by the Wnt/β-catenin signaling pathway. TOPGAL mice are genetically engineered mice in which transcriptional activation of β-
catenin, results in the production of an enzyme, β-galactosidase. The
presence of this enzyme allows us to localize transcriptional
activation of β-catenin to individual cells, thereby, allowing us to quantify the effects that mechanical loading has on the Wnt/β-catenin pathway and new bone formation. The ulnae of loaded TOPGAL
mice were excised and transverse slices along different parts of the
ulnar shaft were assayed for the presence of β-galactosidase.
Our results indicate that loading increases β-catenin transcriptional
activity in regions where this pathway is already primed (i.e. where basal activity is already higher) in a load magnitude dependent
manner. Further experiments are needed to determine the temporal and spatial activation of this signaling in relation to bone formation.},
	    journal   = {International Journal of Biomedical and Biological Engineering},
	  volume    = {3},
	  number    = {10},
	  year      = {2009},
	  pages     = {286 - 288},
	  ee        = {https://publications.waset.org/pdf/761},
	  url   	= {https://publications.waset.org/vol/34},
	  bibsource = {https://publications.waset.org/},
	  issn  	= {eISSN: 1307-6892},
	  publisher = {World Academy of Science, Engineering and Technology},
	  index 	= {Open Science Index 34, 2009},
	}