Wednesday, November 6, 2013

Guest blogger Alan Trounson — October’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.
Scientists in Cincinnati have found how the stem cells that create the blood an immune system age.
Three studies in this month’s report continue the trend of providing concrete examples of the power of iPS type stem cells to model disease. Because they can be made by reprogramming skin, blood or other adult cells from a patient to act like embryonic stem cells, the process can create cell lines with the same genetics as people with the disease. Those cells can then be used to figure out the genetic and molecular causes of the disease. This month teams published work doing this for a type of autism (blogged about here), Parkinson’s disease and blood cancers.

Another team, however, published the most intriguing paper this month. They seem to have unlocked a mystery in the field. As we age our blood-forming, or hematopoietic, stem cells age too and don’t do their job as well as when we are younger. A team led by Hartmut Geiger at Cincinnati Children’s Hospital report finding what could be the master switch that sets in motion the aging of the stem cells.

The researchers began by looking at a molecular pathway called Wnt signaling that has been implicated in aging in other tissues, notably muscle, but had not previously been linked to aging in the vital blood stem cells. They found that older stem cells over produced one of the Wnt path signals. When they artificially over produced that protein in young blood stem cells, those cells behaved more like old ones, less able to produce all the needed components of our blood. Conversely, when they bred mice so that they could not produce the Wnt signal, the blood stem cells continued to perform like young ones even as the animals aged.

The current work builds on another study the group published last year that showed another protein also impacts the aging of blood stem cells. But that protein acts downstream from the Wnt signal in the cascade of events that leads to a poorly functioning blood system. They now need to find out if the Wnt signal is indeed the master switch at the beginning of the pathway and what environmental trigger causes it to be produced in such large quantities it launches the cascade that results in aging cells. But the pathway becomes an immediate target for searching for drugs that could give some youth to older blood stem cells.

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

Alan Trounson

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