2023 Fiscal Year Annual Research Report
Elucidating the role of IL-1R2, a decoy receptor of IL-1, in inflammation-induced stem cell aging
| Project/Area Number |
22K15126
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| Research Institution | Kumamoto University |
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Principal Investigator |
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| Project Period (FY) |
2022-04-01 – 2024-03-31
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| Keywords | Il1r2 / Dlx1 / TPA / skin inflammation |
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| Outline of Annual Research Achievements |
We have successfully generated mouse models with Il1r2 overexpression (pTRE-Il1r2/Rosa-rtTA). In these mice, Il1r2 overexpression mitigated TPA-induced skin inflammation, leading to reduced epidermal thickness, cell proliferation, and inflammatory cytokines (Il1a) when compared to wild-type control mice. Conversely, Il1r2-KO (Il1r2CreERT2) mice did not exhibit phenotypes under basal conditions or TPA-induced skin inflammation compared to their wild-type counterparts.
To observe the behavior of Il1r2-expressing basal cells in tail skin during TPA-induced skin inflammation, we utilized Il1r2CreERT2/Rosa-Td(ts) mouse models. Whole-mount staining of the tail skin revealed that, during TPA-induced inflammation, the size of Il1r2-expressing clones (Il1r2 clones) increased in comparison to Ethanol-treated tail skin. Immunofluorescence staining of tail skin sections demonstrated that under TPA-induced inflammation, Il1r2 clones at the basal layer underwent proliferation and migration toward the upper layers of the tail skin. Notably, under TPA-induced skin inflammation, the behavior of Il1r2 clones differed from that of Dlx1 clones (unpublished), a slow-cycling IFESC population (Sada et al., NCB 2016), indicating that Il1r2 clones at the basal layer may represent a distinct stem cell population.
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