Impaired growth of pancreatic exocrine cells in transgenic mice expressing human activin betaE subunit |
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Authors: | Hashimoto Osamu Ushiro Yuuki Sekiyama Kazunari Yamaguchi Osamu Yoshioka Kazuki Mutoh Ken-ichiro Hasegawa Yoshihisa |
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Affiliation: | Laboratory of Experimental Animal Science, Faculty of Veterinary Medicine, Kitasato University, School of Veterinary Medicine and Animal Sciences, Towada, Aomori 034-8628, Japan. ohashim@vmas.kitasato-u.ac.jp |
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Abstract: | Activins, TGF-beta superfamily members, have multiple functions in a variety of cells and tissues. Recently, additional activin beta subunit genes, betaC and betaE, have been identified. To explore the role of activin E, we created transgenic mice overexpressing human activin betaE subunit. There were pronounced differences in the pancreata of the transgenic animals as compared with their wild-type counterparts. Pancreatic weight, expressed relative to total body weight, was significantly reduced. Histologically, adipose replacement of acini in the exocrine pancreas was observed. There was a significant decrease in the number of PCNA-positive cells in the acinar cells, indicating reduced proliferation in the exocrine pancreas of the transgenic mice. However, quantitative pancreatic morphometry showed that the total number and mass of the islets of the transgenic mice were comparable with those of the nontransgenic control mice. Our findings suggest a role for activin E in regulating the proliferation of pancreatic exocrine cells. |
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Keywords: | Activin E Hypoplasia Pancreatic acinar cell TGF-β superfamily |
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