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In a new study conducted with diabetic mice, human stem cells not only repaired insulin-producing cells in the rodents, they also fixed cells in damaged kidneys.
"It looks like we are doing two things, lowering blood sugar and sending cells to the kidney," said study senior author Dr. Darwin Prockop, director of the Center for Gene Therapy at Tulane University Health Sciences Center in New Orleans. "That's very exciting because there are about 8 million people out there with diabetes and kidney damage and nothing to offer in the way of treatment," Prockop added.
"It's an interesting, novel finding, although obviously some more work needs to be done," added Dr. Rohit N. Kulkarni, an assistant professor of medicine at Harvard Medical School, and head of his own lab in the section on cellular and molecular physiology at the Joslin Diabetes Center, both in Boston. "We are still many steps from figuring out what's happening in humans, but this is one step towards realizing the goal of trying to figure out what stem cells do."
Mesenchymal stem cells or multipotent stromal cells (MSCs) hold quite a bit of promise because they are easily obtained from a patient's bone marrow, grow readily in culture and present minimal immune-system difficulties, the researchers said.
"We're calling them adult stem or progenitor cells. They're not quite entirely stem cells but close to it," Prockop said. "They have a remarkable ability to heal tissues."
"They're part of a natural repair system. Everyone has these cells, but we develop diseases when we don't have enough," he continued. "We can make millions in the laboratory in a matter of three weeks. They speed up the whole repair process."
For this study, published in this week's issue of Proceedings of the National Academy of Sciences, Prockop's team injected human stem cells into mice who had been made diabetic. Another group of mice, the control animals, received no treatment.
Three weeks later, the mice that received the stem cells had higher levels of mouse insulin (not human insulin) than the control mice. "The human cells went to the pancreas and repaired the insulin-producing cells, so the mice began to produce more mouse insulin," Prockop explained. "The human cells went to the pancreas, but it was mouse insulin in the blood stream."
Kulkarni added, "It's intriguing that they enhanced the production of mouse insulin."
Some of the human stem cells also evolved into kidney endothelial cells, or cells that line the interior of blood vessels, and were able to stop damage to the part of the kidney that filters blood. "We also saw human cells in the kidney, and they looked as though they repaired damage to the kidney," Prockop said.
Prockop said the group is now preparing for clinical trials with humans, although other experts still have many questions about the potential therapy.
"This is a very exciting story," said Robert Schwartz, director of the Texas A&M Health Science Center Institute of Biosciences and Technology in Houston. "The issue I take with the article is it's a little like a black box in that we don't understand the mechanism involved, although it's clear from the data that here is an important effect. There are big questions. How long does the effect last? We just don't understand the mechanism, but there's something here of great value," he said.
Insulin, a hormone produced in the pancreas, is needed to carry blood sugar to cells for energy. In people with type 1 diabetes, the pancreas no longer makes insulin. In people with type 2 diabetes, insulin is produced, but their bodies don't respond well to it.
SOURCES: Darwin Prockop, M.D., Ph.D., director, Center for Gene Therapy, Tulane University Health Sciences Center, New Orleans; Rohit N. Kulkarni, M.D., Ph.D., Section on Cellular and Molecular Physiology, Joslin Diabetes Center, and assistant professor, medicine, Harvard Medical School, Boston; Robert Schwartz, Ph.D., director, Texas A&M Health Science Center Institute of Biosciences and Technology, Houston; Nov. 6-10, 2006, Proceedings of the National Academy of Sciences
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