TGF-B in jaw tumor fluids induces RANKL expression in stromal fibroblasts.
| Project/Area Number |
25893125
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Surgical dentistry
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| Research Institution | Okayama University (2014-2015)
Osaka University (2013) |
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Principal Investigator |
Yamada Chiaki 岡山大学, 医歯(薬)学総合研究科, 助教 (80548818)
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| Project Period (FY) |
2013-08-30 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 歯原性腫瘍 / 角化嚢胞性歯原性腫瘍 / エナメル上皮腫 / TGF-β / IL-１α / RANKL / IL-1α / 顎骨腫瘍 |
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| Outline of Final Research Achievements |
Odontogenic tumor, especially Ameloblastomas and KCOT develop in the jaw bone along with bone resorption. The mechanism involves the wide reception of compression-induced bone resorption associated with tumor growth. However,the mechanism of bone resorption in early-stage lesions may not be caused by compression-induced bone resorption.We hypothesized that bone resorption occurs because of RANKL expression mediation in stromal fibroblasts in the jaw bone. In the present study,the expression of TGF-β and IL-1α in odontogenic tumor cells, high concentration of TGF-β in lesion fluid, and synergistic induction of RANKL expression in stromal fibroblasts by TGF-β and IL-1α have been observed. Our results revealed the following two mechanisms: in stromal fibroblasts, TGF-β (1) promotes IL-1 signal-induced NF-κB phosphorylation and promotes RANKL expression and (2) promotes human RANKL transcription activity.
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Report
(3 results)
Research Products
(5 results)
