Stem Cell Image of the Week: Artificial embryos for studying miscarriage (Adonica Shaw)
This week’s stem cell image of the week comes from a team of researchers from The University of Cambridge who published research in Nature Cell Biology earlier this week indicating they’d achieved a breakthrough in stem cell research that resulted in the generation of a key developmental step that’d never before been achieved when trying to generate an artificial embryo.
To create the artificial embryo, the scientists combined mouse embryonic stem cells with two other types of stem cells that are present in the very earliest stages of embryo development. The reseachers grew the three stem cell types into a dish and coaxed them into simulating a process called gastrulation – one of the very first events that happens during a creature’s development in which the early embryo begins reorganizing into more and more complex multilayer organ structures.
In an interview with The Next Web (TNW), Professor Magdalena Zernicka-Goetz, who led the research team, says:
”Our artificial embryos underwent the most important event in life in the culture dish. They are now extremely close to real embryos. To develop further, they would have to implant into the body of the mother or an artificial placenta.”
The goal of this research isn’t to create mice on demand. Its purpose is to gain insights into early life development. And that could lead to a giant leap in our understanding of what happens during the period in a woman’s pregnancy where the risk of miscarriage is highest.
According to professor Zernicka-Goetz,
“We can also now try to apply this to the equivalent human stem cell types and so study the very earliest events in human embryo development without actually having to use natural human embryos.The early stages of embryo development are when a large proportion of pregnancies are lost and yet it is a stage that we know very little about. Now we have a way of simulating embryonic development in the culture dish, so it should be possible to understand exactly what is going on during this remarkable period in an embryo’s life, and why sometimes this process fails.”
Muscle repair cells go rogue – a possible drug target for ALS?
Call it a case of a good cell gone bad. This week researchers at Sanford Burnham Prebys Medical Discovery Institute, report in Nature Cell Biology that fibro-adipogenic progenitors (FAPs) – cells that are critical in coordinating the repair of torn muscles – can turn rogue, causing muscles to wither and scar. This “Dr. Jekyl and Mr. Hype” discovery may lead to novel treatments for a number of incurable disorders like amyotrophic lateral sclerosis (ALS), spinal muscular atrophy (SMA) and spinal cord injury.
When muscle is strained, whether due to an acute injury or even weight-lighting, a consistent order of events occurs within the muscle. FAB cells enter the muscle tissue after immune cells called macrophages come in and gobble up dead tissue but before muscle stem cells are stimulated to regenerate the lost muscle. However, to the researchers’ surprise, something entirely different happens in the case of neuromuscular disorders like ALS where nerve signal connections to the muscles degenerate.
Once nerves are no longer attached to muscle and stop sending movement signals from the brain, the macrophages don’t infiltrate the muscle and instead the FAPs pile up in the muscle and never leave. And as a result, muscle stem cells are never activated. In ALS patients, this cellular train crash leads to progressive loss of muscle control to move the limbs and ultimately even to breathe.
The promising news from these findings, which were funded in part by CIRM, is that the team identified of an out-of-whack cell signaling pathway that is responsible for the breakdown in the rogue function of the FAP cells. The researchers hope further studies of this pathway’s role in muscle degeneration may lead to novel therapies and disease-screening technologies for ALS and other motor neuron diseases.