Here are some stem cell stories that caught our eye this past week. Some are groundbreaking science, others are of personal interest to us, and still others are just fun.
Major advance in getting stem cells to behave. The promise of embryonic stem cells comes from their ability to become any cell type in the body, but medical uses of the cells have been hampered by our poor ability to quickly get them to mature into pure populations of a desired adult tissue. Scientists at Stanford, partially funded by CIRM, and the Genome Institute of Singapore have teamed up to better understand the normal road map of how the various tissues develop in the embryo and in turn fine tune the recipes used to make specific tissues in the lab. They claim to have created pure colonies of 12 different specialized tissues in half the time or less of normal procedures, which usually result in an undesired mix of cells.
“The problems of making or isolating pure samples of one specific cell type has been a substantial barrier to medical uses of embryonic stem cells. This research looks like a way around that problem,” said Hank Greely, a medical ethicist at Stanford not involved in the work in an article in the East Bay Times.
This is a problem researchers around the world have been trying to crack since human embryonic stem cells were first isolated in 2008. The brief paragraph above on how they did it does not do justice to a very elegant and complex research project led by one of the leaders of the field, Irving Weissmann. Stanford’s press release provides more detail about how they achieved the milestone, which should significantly accelerate the field of regenerative medicine.
Mini brains to figure out oversize brains. The many forms of autism have many different causes—though most are unknown—and a wide array of symptoms and physical manifestations. An international team has used a lab dish “mini-brain” model to discover the cause of one form of autism, one linked to over-sized brains, which occurs in about 20 percent of children with autism spectrum disorder (ASD).
A team led by Alysson Muotri at the University of California, San Diego (UCSD), started with tissue samples from children with the disorder and reprogrammed them into iPS type stem cells. They matured those stem cells, first into nerve progenitors and then into the various nerves that in normal cells would result in mini-brains in the lab dish. But instead of a healthy mix of cells that promote and inhibit nerve growth, they found a lack of inhibitory nerves allowing the overgrowth seen in the condition. They also showed the nerve cells did not send signals to each other properly; they lacked synchronization.
“The bottom line is that we can now effectively model idiopathic ASD using a cohort of individuals selected by a clear endophenotype. In this case, brain volume,” said Muotri, in a university press release posted by Health Canal. “And early developmental brain enlargement can be explained by underlying molecular and cellular pathway dysregulation, leading to altered neuronal cortical networks.”
More important, they treated the nerves in the dish with a drug, IGF-1, that is currently being tested in the clinic for autism, and found a reversal of the nerve miss-firing in some of the samples. Their model should make it easier to test more potential drugs, as well.
It has been a big week for improved understanding of ASD. Earlier in the week Fred Gage’s team across the street from UCSD at the Salk institute—where Muotri worked as a post-doctoral fellow—published a causal link for another form of autism, which my colleague Karen Ring wrote about earlier this week in The Stem Cellar.
Help for weekend warriors. How many of your friends have ended up on crutches after a weekend of too much basketball or tennis, with a diagnosis of a torn ligament or tendon? And have they said they wished they had broken a bone instead because it would heal faster? Medicine has not been able to speed the healing of those delicate connecting straps in large part because we haven’t known much about how they are created during development. So a team at the Scripps Research Institute set out to find out how they develop and heal naturally.
“If we understand the molecular mechanisms of tendon development, we can apply the findings to develop a new regenerative therapy for tendon diseases and injuries,” said team leader Hiroshi Asahara in an institution release posted by Sciencecodex.
They found one gene in particular linked to tendon development and repair in an animal model. They used the new trendy gene editing tool CRISP to regulate the gene in rats. They found the gene results in the production of more tenocytes, which are needed to maintain healthy tendon. That pathway now becomes a target for developing new therapies to help those hobbling friends.
For the follicular challenged. On a lighter note, one of the least impactful but most common medical conditions, hair loss, has become a target of therapy development by many university and industry teams. Forbes posted a run down about the activities of some of the leaders of the hair pack.
Not all the author’s science is spot on, for example, when talking about the only organs that constantly regenerate the author ignored the fact that our gut lining turns over about every four days. But he provides a good review of how our hair follicles generally do a good job of replenishing hair and what goes wrong when they fail.
The author focuses most on the work of Japan’s RIKEN Institute, providing an easy to follow info-graphic on how the team there envisions harvesting a small skin sample, sorting the stem cells out of the hair follicles in the sample, growing those stem cells in the lab many fold and then injecting cells back to where they are needed. That team hopes to have a commercial product by 2020. In the meantime, the top of my head will remain intimately acquainted with sun screen.