Stem cell photo of the week:
Recreating brain cell interactions for studying schizophrenia
Our pick for the stem cell image of the week is from the laboratory of Rusty Gage at the Salk Institute. The team generated multiple types of nerve cells from stem cells to more closely represent the interactions that occur in the brain. They’re using this system to show how the communication between these nerve cells becomes faulty in people with schizophrenia. A Salk Institute press release provides more details about their study which was published in Cell Stem Cell.
Regenerative power of intestinal stem cells maintained via fasting
For many decades, researchers have known that restricting food intake in mice can extend life span. Why it happens hasn’t been well understood. This week, a team at MIT uncovered a possible explanation: fasting increases the regenerative power of stem cells.
The report, published in Cell Stem Cell, focused on the well-studied intestinal stem cell, which renews the intestinal lining every five days. As we age, the intestinal stem cell’s regenerative abilities wane and damage to the intestinal lining takes longer to repair.
Mice were fasted for 24 hours and then their intestinal stem cells were retrieved and grown into mini-intestine organoids in petri dishes. According to Maria Mihaylova, PhD, one of the lead authors, the results of the experiment were very clear:
“It was very obvious that fasting had this really immense effect on the ability of intestinal crypts to form more organoids, which is stem-cell-driven,” Mihaylova said in a press release. “This was something that we saw in both the young mice and the aged mice, and we really wanted to understand the molecular mechanisms driving this.”
Mihaylova and the team went on to show that fasting caused the stem cells to burn fat instead of carbohydrates for their energy needs. Inhibiting the gene pathways that flip this metabolic switch also blocks the regenerative capacity of fasting. On the other hand, molecules that boost the gene pathways mimic the effects of fasting without changing food intake. This intriguing finding could potentially have clinical applications for cancer patients who suffer intestinal injury from the toxic effects of chemotherapy drugs but who certainly aren’t in a condition to fast.
Premature graying, our immune system and stem cells: a surprising link. (Kevin McCormack)
As someone whose hair went gray at a relatively young age – well, it seemed young to me! – this next story naturally caught my eye. It highlights how our immune systems may play a key role in determining our hair color and, in particular, when that hair turns gray.
Our bodies are constantly shedding hairs and replacing them with new ones. Normally stem cells called melanocytes help ensure the new hairs have your original color, be it black, blonde, brunette or red.
Researchers at the National Institutes of Health and the University of Alabama, Birmingham, found that when the body is attacked by a virus, our immune system kicks in and respond by producing interferon to fight off the infection. However, when a protein called MITF, that is involved in regulating how cells use interferon, fails to work properly it can also affect melanocytes causing them to lose their pigmentation. Without that pigmentation the new hairs are gray.
The study, which appears in the journal PLOS Biology, is too late to help me and my gray hair – particularly as it was done in mice – but it could pave the way for further research that identifies how genes that control pigment in our hair and skin also control our immune system.
One thought on “Stem Cell Roundup: better model of schizophrenia, fasting boosts stem cells, and why does our hair gray.”
More care should be used to avoid untrue generalizations:
“For many decades, researchers have known that restricting food intake in humans … leads to extended life spans.”
This statement is simply not true. It is a speculation based on animal studies, but unproven for humans to date.
And the cited paper’s interpretation of its findings is similarly erroneous. Stem cells may play a role in intestinal organoid growth, but they have not been shown to be rate-determining for organoid growth. In addition, the biomarkers used to assign stem cell character in these studies lack sufficient specificity to make such designations, as they also identify committed progenitor cells which greatly outnumber stem cells. The observed effects in fasted mice certainly involve committed progenitor cells; but whether stem cell effects are also involved is an unsubstantiated proposition, which could be wrong.
A major, continuing problem that undermines the quality and progress of stem cell science is the lack of technical and biological exactness, in a field of biomedical research that has a unique need for it.
James @ Asymmetrex