2002 Fiscal Year Final Research Report Summary
Regulation of gene expression by D-amino acids
| Project/Area Number |
13672296
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | Kitasato University |
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Principal Investigator |
HOMMA Hiroshi Kitasato University, School of Pharmaceutical Sciences Professor, 薬学部, 教授 (50190278)
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| Project Period (FY) |
2001 – 2002
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| Keywords | D-Aspartate / testosterone / Steroidogenic acute regulatory protein / Leydig cells / steroidogenesis / glutamate transporter / mLTC-1 cells |
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| Research Abstract |
We have reported that D-aspartate (D-Asp) increases human chorionic gonadotropin (hCG)-induced testosterone production in purified rat Laydig cells. D-Asp is presumed to be taken up into the cells and increases the protein and mRNA levels of Steroidogenic acute regulatory protein (StAR), which is an essential protein for the steroidogenesis. We found in this study that D-Asp increases StAR protein expression in mLTC-1 cells (mouse Leydig Tumor Cell-1), a cultured cell line that would be a suitable model of rat Leydig cells. In these cells, D-Asp promotes StAR protein expression only when the cells transiently express glutamate transporter, through which D-Asp is taken up into the cells. This result shows that D-Asp uptake is necessary for the stimulation of StAR gene expression. In addition, D-Asp stimulates StAR protein expression in the cells which stably express glutamate transporter, while it did not promote the protein expression in the parent mLTC-1 cells. These lines of evidence show that D-Asp should be taken up into mLTC-1 cells before it stimulates StAR gene expression. Details should be clarified on the mechanism of D-Asp stimulation of StAR gene expression in mLTC-1 cells.
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