Durham, NC – A new study appearing in STEM CELLS Translational Medicine (SCTM) shows how understanding the way a type of molecule called CD133 functions might contribute to an understanding of the mechanisms involved in kidney repair.
Kidney injuries affect up to 7 percent of hospitalized patients, with those in intensive care especially vulnerable. An increasing amount of evidence indicates that although the kidney might seem to regain normal function, in fact it remains permanently damaged.
Studies conducted on mice have shown that stem cell therapy is a possible path to total kidney repair. That’s why scientists are interested in the CD133 molecule.
“In the human kidney, the expression of CD133 characterizes a population of cells with the ability to proliferate — with the added benefit of showing a resistance to damage,” said Benedetta Bussolati, M.D., Ph.D., of the University of Torino’s Molecular Biotechnology Centre and the SCTM study’s lead investigator. “But not much was known about how CD133 functions. So we aimed to evaluate this as well as CD133’s possible implication in the repair process.”
Their work led them to discover that CD133 may act as a permissive key factor for β-catenin signaling, which can control cell proliferation, survival, cell behavior and cell fate in both embryos and adults. These findings represent a potential application for kidney tissue repair/regeneration.
“This is an interesting and novel finding,” said Anthony Atala, M.D., Editor-in-Chief of STEM CELLS Translational Medicine and director of the Wake Forest Institute for Regenerative Medicine. “Because the work identifies mechanisms potentially involved in the repair of tissue after injury, it suggests the possibility of new therapies for tissue repair and regeneration.”
The full article, “Role of CD133 Molecule in Wnt Response and Renal Repair,” can be accessed at: http://www.stemcellstm.com.