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Islet Endothelial Cells and Pancreatic ß-Cell Proliferation: Studies in Vitro and during Pregnancy in Adult Rats

Departments of Medical Cell Biology (M.J., G.M., A.A., L.J., P.-O.C.) and Medical Sciences (P.-O.C.), Uppsala University, SE-751 23 Uppsala, Sweden; and Biomedical Research Institute, Department of Biological Sciences, University of Warwick (G.M.), Warwick CV4 7AL, United Kingdom

Address all correspondence and requests for reprints to: Dr. Magnus Johansson, Department of Medical Cell Biology, Biomedical Center, Husargatan 3, Box 571, SE-751 23 Uppsala, Sweden. E-mail: magnus.johansson{at}medcellbiol.uu.se.

The growth of both tumors and nonneoplastic tissues may be influenced by signals from the vascular endothelium. In the present investigation we show that purified proliferating endothelial cells from pancreatic islets can stimulate ß-cell proliferation through secretion of hepatocyte growth factor (HGF). This secretion could be induced by soluble signals from the islets, such as vascular endothelial growth factor-A (VEGF-A) and insulin. During pregnancy, the pancreatic ß-cells display a highly reproducible physiological proliferation. We show that islet endothelial cell proliferation precedes ß-cell proliferation in pregnant animals. Vascular growth was closely associated with endocrine cell proliferation, and prominent expression of HGF was observed in islet endothelium on d 15 of pregnancy, i.e. coinciding with the peak of ß-cell proliferation. In summary, our results suggest the existence of an endothelial-endocrine axis within adult pancreatic islets, which is of importance for adult ß-cell proliferation.

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