More on Lin28a and Enhanced Regeneration

Here is a better set of publicity materials describing recent research in which scientists demonstrated enhanced regeneration in mice:

By reactivating a dormant gene called Lin28a, which is active in embryonic stem cells, researchers were able to regrow hair and repair cartilage, bone, skin and other soft tissues in a mouse model. Lin28, first discovered in worms, functions in all complex organisms. It is abundant in embryonic stem cells, expressed strongly during early embryo formation and has been used to reprogram skin cells into stem cells. It acts by binding to RNA and regulating how genes are translated into proteins. [The] researchers found that Lin28a also enhances the production of metabolic enzymes in mitochondria, the structures that produce energy for the cell. By revving up a cell's bioenergetics, they found, Lin28a helps generate the energy needed to stimulate and grow new tissues.

"Efforts to improve wound healing and tissue repair have mostly failed, but altering metabolism provides a new strategy which we hope will prove successful. Most people would naturally think that growth factors are the major players in wound healing, but we found that the core metabolism of cells is rate-limiting in terms of tissue repair. The enhanced metabolic rate we saw when we reactivated Lin28a is typical of embryos during their rapid growth phase."

"We already know that accumulated defects in mitochondrial metabolism can lead to aging in many cells and tissues. We are showing the converse - that enhancement of mitochondrial metabolism can boost tissue repair and regeneration, recapturing the remarkable repair capacity of juvenile animals." Further experiments showed that bypassing Lin28a and directly activating mitochondrial metabolism with a small-molecule compound also had the effect of enhancing wound healing. This suggests the possibility of inducing regeneration and promoting tissue repair with drugs.

Link: http://www.sciencedaily.com/releases/2013/11/131107123144.htm