Elucidation of the mechanism underlying apoptosis-induced compensatory proliferation using a murine model
| Project/Area Number |
25670167
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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 |
Pathological medical chemistry
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| Research Institution | Toho University (2014)
Juntendo University (2013) |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 細胞死 / cFLIP / アポトーシス / ネクロプトーシス / 腸炎 / X染色体不活性化 / 代償性増殖 / ノックインマウス / RegIII / X染色体 / マイクロアレイ / Crisper/Cas9 / cFLIPs / トランスジェニックマウス |
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| Outline of Final Research Achievements |
Apoptotic cells might produce growth factors that subsequently induce proliferation, which is referred to as compensatory proliferation. The aim of the study is to identify growth factors released from dying cells and elucidate the mechanisms underlying compensatory proliferation. We generated mice that harbored cFLIPs gene at a locus on X chromosome. Intestinal epithelial cells of cFLIPs KI mice underwent apoptosis, however, female cFLIPs KI mice were born and developed without abnormality, and fertile. To identify candidate genes that are potentially involved in proliferation, we performed genome-wide transcriptome analysis using intestines of cFLIPs KI embryos and we found that RegIIIb and RegIIIg involved in tissue repair were significantly elevated in the intestine of cFLIPs KI embryos compared to wild-type embryos. Now, we are going to generate mice lacking both RegIIIb and RegIIIg to elucidate a role for these genes in compensatory proliferation.
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Report
(3 results)
Research Products
(28 results)
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[Journal Article] Disruption of Tumor Necrosis Factor Receptor Associated Factor 5 Exacerbates Pressure Overload Cardiac Hypertrophy and Fibrosis.2014
Author(s)
Bian, Z., Dai, J., Nakano, H., Guan, H., Yuan, Y., Gan, L., Zhou, H., Zong, J., Zhang, Y., Li, F., Yan, L., Shen, D., Li, H., and Tang, Q.
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Journal Title
J Cell Biochem
Volume: 115
Issue: 2
Pages: 349-358
DOI
Related Report
Peer Reviewed
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