StemCell Therapy

Public release date: 23-Apr-2012 [ | E-mail | Share ]

Contact: Andrea Boyle Tippett aboyle@udel.edu 302-831-1421 American Society for Biochemistry and Molecular Biology

Biology Major Adam Reese may have found the key to keep fat cells from forming.

The University of Delaware junior believes he has identified the trigger that turns a stem cell into a fat cell. Located on the surface of cells, the trigger, a protein called endoglin, regulates what type of cell an existing stem cell will become.

Working in the biological science department's laboratory of cellular signaling and dynamics with Assistant Professor Anja Nohe, Reese investigates ways to combat osteoporosis; his findings may also have implications for obesity.

Reese will present his work at 12:25 p.m. Monday at the American Society for Biochemistry and Molecular Biology's annual meeting, which is being held in San Diego in conjunction with the Experimental Biology 2012 conference.

Patients afflicted with osteoporosis lose bone mass as they age. Bone is a dynamic tissue, constantly renewed by removal or reabsorption of old bone and formation of new bone. Through this cellular remodeling process, roughly one fifth of an adult's skeleton is replaced each year. Of the limited treatments developed to reduce bone loss, most have potentially serious side effects, are cost prohibitive or difficult to use.

Reese, with the help of graduate student Joyita Dutta, found the amount of endoglin on a cell's surface indicates whether the cell will become a fat cell or a bone cell.

"What would happen if you could make the cell stop making the protein?" Reese said. "You could affect whether or not it's even a fat cell."

If the amount of endoglin on the cell surface could be decreased, the amount of cells turning into bone would rise, leading to an increase in bone strength, thus ending osteoporosis.

Originally posted here:
The fat stopper

This entry was posted on April 25, 2012 at 7:12 pm and is filed under Fat Stem Cells. You can follow any responses to this entry through the RSS 2.0 feed. Both comments and pings are currently closed. |