1995 Fiscal Year Final Research Report Summary
Local Regulation of Endocrine Organ by Members of TGF family
| Project/Area Number |
05454315
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
内分泌・代謝学
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| Research Institution | Gunma University |
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Principal Investigator |
KOJIMA Itaru Professer, Department of Cell Biology, Institute for Molecular and Cellular Regulation, Gunma University, 生体調節研究所, 教授 (60143492)
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| Co-Investigator(Kenkyū-buntansha) |
SHIBATA Hiroshi Associate Professor, ibid., 生体調節研究所, 助教授 (20235584)
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| Project Period (FY) |
1993 – 1995
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| Keywords | TGF-beta / activin A / pancreatic endocrine cell / differentiation / insulin / calcium / autocrine / paracrine |
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| Research Abstract |
In the present research, we studied the role of members of TGF-beta supergene family in the regulation of pancreatic endocrine cell. We obtained the following results. First, we showed that activin A and TGF-beta are expressed in non-beta and beta-cells of the pancreatic islet, reapectively. Second, both activin A and TGF-beta stimulate insulin secretion by calcium-dependent manners. Furthermore, these two ligands inhibit the activity of the ATP-sensitive potassium channel and increase calcium influx via voltage-dependent calcium channel. This mode of action resembles that of glucose, a major stimulant of insulin secretion. Third, activin A is expressed in endocrine precursor cells found in pancreatic anlage and is thought to play a role in the differentiation of pancreatic endocrine cells. Consistent with this notion, activin A converted amylase-containing pancreatic AR42J cells, a cell line possessing characteristics similar to pancreatic precursor cells, into neuron-like cells. Furthermore, activin A-treated AR42J cells express pancreatic polypeptide, a pancreatic hormone. Hence, activin A converts AR42J cells into endocrine cells in pancreas.
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