Study identifies protein responsible for mechanism behind bone loss

In this study, the researchers set out to better understand RANKL’s role in directing osteoclasts to promote bone loss and whether there could be a way to control the pathway toward bone regeneration or bone growth.METHODThe researchers focused their study on the autophagy, or cellular regeneration process, in osteoclasts in order to figure out why RANKL promotes bone loss. It is well-known that autophagy becomes activated primarily during cellular stress, such as starvation. However, there is growing evidence that shows autophagy can be activated through signaling pathways and that cellular functions could be controlled.They started by examining Beclin1, an indispensable protein for autophagy initiation, in combination with RANKL-activated cells, both in  in vitro cell work and in in vivo (in the living organism) studies of mice. The team evaluated several models of Beclin1-enhanced combinations and came to the conclusion that an overexpression of the Beclin1 protein was directly tied to cells changing into osteoclasts. They went one step furthe r by developing a mouse model where they eliminated Beclin1 in osteoclasts and the results were thicker cortical bone, which is bone tissue that’s denser than other types and accounts for up to 80% of the weight of a human’s skeleton.IMPACTAccording to the National Osteoporosis Foundation, experts predict that by 2025, osteoporosis will be responsible for 3 million fractures, resulting in $25.3 billion in health care-relate...
Source: UCLA Newsroom: Health Sciences - Category: Universities & Medical Training Source Type: news