Spleen mesenchymal cells incorporated into the pancreatic microenvironment
| Project/Area Number |
26660259
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Integrative animal science
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| Research Institution | Tokyo University of Science |
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Principal Investigator |
GOITSUKA RYO 東京理科大学, 研究推進機構生命医科学研究所, 教授 (50301552)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 間葉系細胞 / 幹細胞 / 再生 / 発生 / 微小環境 / 免疫 / 脾臓 / 膵臓 / 再生医学 / 転写因子 |
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| Outline of Final Research Achievements |
Tlx1 is an essential transcription factor for spleen organogenesis. We have demonstrated by genetic lineage-tracing of Tlx1-expressing cells and their progeny using Tlx1CreER-Venus;Rosa26-tdTomato mice that Tlx1 deficiency causes these cells to be incorporated into the dorsal pancreatic mesenchyme, where they give rise to desmin- and vimentin-positive cells scattering around the endocrine, exocrine and ductal cells. By using the embryonic gut organ culture system, we observed that Tlx1-expressing descendants expanded in spleno-pancreatic mesenchyme through the mesenchyme overlying the stomach from the posterior to anterior direction. In contrast, individual cells of the Tlx1-deficient spleno-pancreatic mesenchyme appeared to migrate randomly. These findings suggest that the Tlx1-deficient progeny derived from precursors, in which Tlx1 was transcriptionally activated, fail to move out from spleno-pancreatic mesenchyme, thus being misallocated to the dorsal pancreas.
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Report
(3 results)
Research Products
(10 results)
