Normal aging is accompanied by a diminished ability to regain strength and mobility after muscle injury because over time stem cells within muscle tissues dedicated to repairing damage become less able to generate new muscle fibers and struggle to self-renew, researchers at Stanford University reported Sunday.
"In the past, it's been thought that muscle stem cells themselves don't change with age, and that any loss of function is primarily due to external factors in the cells' environment," Helen Blau of the university's school of medicine said.."However, when we isolated stem cells from older mice, we found that they exhibit profound changes with age. In fact, two-thirds of the cells are dysfunctional when compared to those from younger mice, and the defect persists even when transplanted into young muscles."
However, Blau and her colleagues say they've identified for the first time a process by which the older muscle stem cell populations can be rejuvenated to function like younger cells.
"Our findings identify a defect inherent to old muscle stem cells," she said. "Most exciting is that we also discovered a way to overcome the defect. As a result, we have a new therapeutic target that could one day be used to help elderly human patients repair muscle damage."
The researchers used drugs to block elevated biological activity within the stem cells that causes them to degenerate into non-stem, muscle progenitor cells.
When transplanted back into the animal, the treated, rejuvenated stem cells migrate to their natural niches and provide a long-lasting stem cell reserve to contribute to repeated demands for muscle repair, they researchers said.
"In mice, we can take cells from an old animal, treat them for seven days -- during which time their numbers expand dramatically, as much as 60-fold -- and then return them to injured muscles in old animals to facilitate their repair," Blau said.