Washington: Researchers have discovered a new target that may be critical for the treatment of osteoporosis.
The group of researchers in The Netherlands and in Germany have found in their studies in zebrafish and mice that injection of human plastin 3 (PLS3) or related proteins in zebrafish where PLS3 action has been suppressed can replace its loss and repair the bone development anomalies associated with this deficiency.
According to the study, over-expression of human (PLS3) in normal mice had a significant impact on bone development and maintenance, making them more resistant to fractures.
Professor Brunhilde Wirth, Head of the Institute of Human Genetics, University of Cologne, Germany, said that in most of their recent research, they have started out by using zebrafish embryos in which PLS3 was knocked-out and studying their development at the three and five day-old stage.
He said that they have found that they had massive impairment of craniofacial skeletal development, however, this was fully restored when they added human PLS3 and the same thing happened when we added two other proteins, actinin 1 and actinin 4, F-actin proteins2 which are involved in 'bundling' or building the 'scaffolding' for cells, and it seems that these proteins can compensate for the loss of PLS3.
The scientists now intend to use PLS3 knock-out mice, where the PLS3 gene has been removed, in the search for the disease-causing mechanism involved.