Scientists have known that developing organs communicate with blood vessels via chemical signals to ensure that they receive the proper blood supply to sustain growth. Now, researchers have discovered that blood vessels themselves can send signals to the pancreas that trigger its development. The finding provides the first glimpse of a new type of biochemical signaling pathway that may prevent the pancreas, and possibly other organs, from developing until a blood-supply pipeline is in place.

According to the researchers, the source of the blood vessel signal may prove useful to scientists who are hoping to guide the differentiation of embryonic stem cells into pancreatic islet cells, the insulin-producing cells that are depleted in people who have type I diabetes. The discovery was published September 28, 2001, in the journal Science, as part of the Science Express Web site.

"Other biologists might already have thought of the possibility of such signaling, but it was definitely a surprise to me," said Melton, a Howard Hughes Medical Institute investigator at Harvard University. According to Melton, insights from histological studies provided the initial evidence that led them to search for blood vessel signaling.

"When we used histological sections to examine how the pancreas develops, what jumped out was that we could never find any evidence for pancreas development or differentiation when there wasnt a blood vessel touching it," he said. "Also, it has been long known that in mice the pancreas develops by initially forming three buds, which are subsequently reduced to two. These remaining two buds fuse to form the whole pancreas. Wed always been puzzled about why the third bud disappears, and our examinations showed that this bud invariably loses its contact with a blood vessel. Taken together, these studies indicated to us that pancreatic development is closely linked with the presence or absence of blood vessels."

Melton and collea
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Contact: Jim Keeley
keeleyj@hhmi.org
301-215-8858
Howard Hughes Medical Institute
27-Sep-2001

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