Guest blogger Alan Trounson — May’s stem cell research highlights

Each month CIRM President Alan Trounson gives his perspective on recently published papers he thinks will be valuable in moving the field of stem cell research forward. This month’s report, along with an archive of past reports, is available on the CIRM website.

I devote most of my report this month to four papers that report significant progress in regenerating the two tissues that make up the bulk of our bodies, bone and muscle. In the past, both have been difficult to grow from stem cells in sufficient quantities to be therapeutically useful.

Two teams grew bone in the lab, one from stem cells found in fat and one from cells derived from embryonic stem cells. Both found that the lab-grown bone grew and matured when transplanted into mice. Two other teams got sufficient muscle regeneration to treat mice with a disease that mimics muscular dystrophy. One started with muscle precursor cells derived from pluripotent stem cells. The other found a protein that could summons naturally occurring putative stem cells called satellite cells and get them to regenerate muscle. (We blogged about those muscle regeneration papers here and here.)

However, the most important of the papers I highlighted this month may be the two that delve into the issue of aging stem cells. We have adult stem cells in most, if not all, the tissues of our bodies that throughout our life get called out of their stem cell niches—sort of store rooms—to make repairs and replace those tissues. Much of the break down of various tissues and loss of organ function that comes with aging is caused by a loss in number of stem cells, or a loss of them to fully function. This has lead many to question whether we can put new stem cells into an aging environment and expect them to do the work we want them to do.

One team this month reported that they had verified the role of a specific protein in the loss of function in blood-forming stem cells. They also showed that a drug-like compound could block the action of that protein and restore old stem cells to functioning like young ones. The other team, mapped a series of signals that start with a molecule sent from the niche cells that result in decreased numbers of stem cells, in at least one setting. They were able to block that pathway and get increased numbers of stem cells.

Both papers reinforce the need to be mindful of the impact of aging on stem cells, but also point to ways to bypass this obstacle. Good news.

My full report is available online, along with links to my reports from previous months.

A.T.