Newts and salamanders have the ability to regrow a lost tail or leg. And now, Stanford researchers may have found a way to recreate this ability in mice, paving the way for potentially regenerating damaged tissues in humans.
"Newts regenerate tissues very effectively," says Helen Blau, the Donald E. and Delia B. Baxter Professor and a member of Stanford's Institute for Stem Cell Biology and Regenerative Medicine. "In contrast, mammals are pathetic. We can regenerate our livers, and that's about it. Until now it's been a mystery as to how they do it."
Blau and her team tried to determine what was different between mammalian and salamander cells when it comes to cell cycle control. One aspect involves a class of proteins called tumor suppressors that block inappropriate cell division. Research has shown that the tumor suppressor retinoblastoma, or Rb, helps prevent many types of specialized mammalian cells, including those found in muscle, from uncontrollably dividing. But blocking the expression of Rb in mammalian cells has been inconsistent; it sometimes allowed the cells to hop back into the cell cycle, but not other times.
The researchers then wondered if another tumor suppressor called ARF might be involved. Indeed, they found that blocking the expression of both tumor suppressors allowed individual myocytes isolated from mouse muscle to dedifferentiate and begin dividing. When they put the cells back into the mice, they were able to merge with existing muscle fibers--as long as Rb expression was restored. The researchers' findings were published recently in the journal Cell Stem Cell.
Separately, researchers at Gladstone Institute of Cardiovascular Disease, San Francisco, say they have converted cells supporting the structure of the heart into beating-heart cells in mice. The finding points to a new way to regenerate heart muscle that is damaged in a heart attack, the Wall Street Journal notes.
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