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The Creation and Analysis of a New Genetic Model of Osteoporosis in Transgenic Mice Overexpressing the RANKL Cytokine
The Creation and Analysis of a New Genetic Model of Osteoporosis in Transgenic Mice Overexpressing the RANKL Cytokine
YEAR
2010
PROGRAMME
Scientific Projects ›
PROGRAMME
Biomedical Sciences Research Center "Alexander Fleming"
PHOTO GALLERY ↓

Osteoporosis is a chronic disease that primarily affects menopausal women and is characterised by low bone mass and increased risk of fractures. RANKL is the main mediator in bone resorption by inducing osteoclast generation. Recently, it was discovered that pharmaceutical inhibition of RANKL effectively prevents bone loss and fractures in osteoporotic patients, making RANKL the most specialised target against osteoporosis.
The research group has recently generated mice that over-produce human RANKL using genetic engineering. The study analyses new genetic models of osteoporosis resulting from the overexpression of human RANKL. Specifically, we characterised two models of osteoporosis in detail, one with low expression of RANKL and mild osteoporosis and one with highly elevated levels of RANKL and characteristics of severe osteoporosis, such as trabecular bone loss, cortical porosity and reduced bone strength.

The administering of a commercial anti-osteoporotic drug in these models showed that bone loss was prevented, making them ideal models for the evaluation of new inhibitors against human RANKL in the preclinical level. The development of these first animal models of osteoporosis induced by overexpression of human RANKL will pave the way for the discovery of highly-specific novel drugs.

 

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