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The Prox1 gene is a key regulator of the embryonic development of the pancreas, according to studies in laboratory models led by a team of St. Jude Children's Research Hospital researchers.
The investigators found that early in the development of the pancreas (before day 11½), the absence of Prox1 severely hindered the growth of the pancreas; and it reduced the number of endocrine cells that produce glucagon, a hormone that raises the level of glucose in the blood. Importantly, after day 13½ of development, this lack of Prox1 caused an abnormal decrease in the number of islet cells that produce insulin.
On the other hand, the absence of Prox1 led to an increase in the number of exocrine cells that developed. Exocrine cells produce digestive enzymes and release them into ducts that lead out of the pancreas.
The researchers concluded from this study that Prox1 plays an important role in triggering the development of an adequate number of islet cells while the pancreas develops; it is possible that Prox1 does this by preventing cells called multipotent pancreatic progenitors from developing into exocrine cells.
"In this way, the embryonic pancreas produces the proper number of islet cells and exocrine cells as it forms," said Beatriz Sosa-Pineda, PhD, St. Jude Genetics and Tumor Cell Biology. She is senior author of a report on this work appearing in the October 1 issue of Developmental Biology.
Other St. Jude authors of the study include Junfeng Wang, Gamze Kilic and Guillermo Oliver, PhD, St. Jude Genetics and Tumor Cell Biology.
St. Jude does both laboratory and clinical research in order to find cures for catastrophic diseases of children. Much of this research, especially in the laboratory, leads to discoveries of the basic workings of the body's cells. Therefore, some of our work has broader implications than childhood diseases and provides insights into adult diseases as well.
Last update: November 2005