Sep. 17, 2013 Scientists have succeeded in growing stem cells that have the ability to develop into two different types of cells that make up a healthy pancreas. The research team led by Dr. Hans Clevers of the Hubrecht Institute, The Netherlands, have isolated and grown stem cells from the pancreases of mice using a 3-D culture system previously developed by the scientists. The results, which are reported in The EMBO Journal, could eventually lead to ways to repair damaged insulin-producing beta cells or pancreatic duct cells.

Cell signalling molecules known as Wnts and a protein called Lgr5 are essential to produce adult stem cells that can be coaxed to grow and divide rapidly. However, these signaling pathways and molecules are inactive in the adult pancreas. "We have found a way to activate the Wnt pathway to produce an unlimited expansion of pancreatic stem cells isolated from mice," Clevers said. "By changing the growth conditions we can select two different fates for the stem cells and generate large numbers of either hormone-producing beta cells or pancreatic duct cells." He added: "This work is still at a very early stage and further experiments are needed before we can use such an approach for the culture of human cells but the results are a promising proof-of-concept."

In the study, the pancreases of mice were altered in a way that makes duct cells proliferate and differentiate. Some cells in this new population were stem cells that were capable of self-renewal. The scientists were able to culture these cells to give rise to large numbers of pancreatic cells or tiny clumps of tissue referred to as organoids.

Therapeutic strategies for pancreatic disease have been hampered by a lack of cell culture systems that allow scientists to grow replacement tissue in a test tube or on a dish. Alternative approaches such as tissue transplantation are limited by the scarcity of donors and the possibility of tissue rejection. The new work offers access to an unlimited supply of pancreatic stem cells that would be beneficial for the development of new therapeutic interventions for pancreatic diseases like diabetes.

The next steps for the scientists will include further refinement of the cell culture methods developed in this study and investigation of ways to extend the approach to human pancreatic cells.

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Pancreatic stem cells isolated from mice

Newswise We often think of human cells as tiny computers that perform assigned tasks, where disease is a result of a malfunction. But in the current issue of Science, researchers at The Mount Sinai Medical Center offer a radical view of health seeing it more as a cooperative state among cells, while they see disease as result of cells at war that fight with each other for domination.

Their unique approach is backed by experimental evidence. The researchers show a network of genes in cells, which includes the powerful tumor suppressor p53, which enforce a cooperative state within cellsrather like the queen bee in a beehive. Disease or disorder occurs when these enforcer genes are mutated, allowing competition between cells to ensue.

Both competition and cooperation drive evolution, and we are wired for cooperation all the way down to our genes, says the studys senior investigator, Thomas P. Zwaka, MD, PhD, Professor at the Black Family Stem Cell Institute at the Icahn School of Medicine at Mount Sinai.

The findings, if backed by future research, offer a new way to address disease, Dr. Zwaka says. Understanding the genetic basis of cooperative and competitive cellular behaviors could explain how cancer and immune system dysfunction develops, he says. If a cell has lost a gene that fosters communication among cells, it may dominate other cells by ignoring signals to stop proliferating. It also makes sense that the immune system might detect and attack cells that are not cooperating. Failure to cooperate may also underlie development of birth defects.

He adds that it may be possible to flip the cooperation switch back on therapeutically, or to manipulate stem-like cells to misbehave in a way that produces replacement cells for regenerative medicine.

Cell misbehave, they are unpredictable. They do not operate like little machines, he says. What our study suggests is that cooperation is so central to our evolution that we have genetic mechanisms to protect us against cheating and dominating behavior.

A network of genes with an ancient function The research team, which also includes study first author Marion Dejosez, PhD, Assistant Professor at the Icahn School at Mount Sinai, took a long view toward the behavior of cells. They wondered how it was that cells, which lived on earth as single units for hundreds of millions of years, could effectively bundle themselves together to perform specific tasks. Cells started somehow to form alliances, and to cooperate, and obviously this multicellularity had certain advantages.

But they also questioned what happened to the cheating behavior that can be seen in single cells, such as amoeba, that live in colonies competitive behavior that allows the cell to gain a reproductive advantage without contributing its fair share to the community.

They conducted a genetic screen in stem cells to look for mutants that allow cells to misbehaveto become a little antisocial and do things they wouldnt normally do, Dr. Zwaka says. The screen picked up about 100 genes, which seem to cluster together into a network.

The team focused on three of those genesp53, long known as the guardian of the genome, Topoisomerase 1 (Top1), which control genomic stability, and olfactory receptors involved in the sensation of smell.

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Stem Cells are Wired for Cooperation, Down to the DNA