The elucidation of the pathophysiology of gingival overgrowth.
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- Yamashita Akiko
- Principal Investigator
- 九州大学
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- 西村 英紀
- Co-Investigator
- 九州大学
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- 岩下 未咲
- Co-Investigator
- 九州大学
About this project
- Japan Grant Number
- JP18K09578
- Funding Program
- Grants-in-Aid for Scientific Research
- Funding organization
- Japan Society for the Promotion of Science
- Project/Area Number
- 18K09578
- Research Category
- Grant-in-Aid for Scientific Research (C)
- Allocation Type
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- Multi-year Fund
- Review Section / Research Field
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- Basic Section 57030:Conservative dentistry-related
- Research Institution
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- Kyushu University
- Project Period (FY)
- 2018-04-01 〜 2022-03-31
- Project Status
- Completed
- Budget Amount*help
- 3,380,000 Yen (Direct Cost: 2,600,000 Yen Indirect Cost: 780,000 Yen)
Research Abstract
SPOCK1 is an extracellular proteoglycan that induces epithelial to mesenchymal transition (EMT) in several cancer cell lines and exhibits protease-inhibitory activity. However, the role of SPOCK1 in non-cancerous diseases such as DIGO has not been well-addressed. We demonstrated that the expression of SPOCK1, TGF-β1, and MMP-9 in calcium channel blocker-induced gingival overgrowth is higher than that in non-overgrowth tissues. Transgenic mice overexpressing Spock1 developed obvious gingival-overgrowth and fibrosis phenotypes, and positively correlated with EMT-like changes. Furthermore, in vitro data indicated a tri-directional interaction between SPOCK1, TGF-β1, and MMP-9 that led to gingival overgrowth. Our study shows that SPOCK1 up-regulation in a noncancerous disease and SPOCK1-induced EMT in gingival overgrowth occurs via cooperation and crosstalk between several potential signaling pathways.
Details 詳細情報について
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- CRID
- 1040282256978094848
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- Text Lang
- ja
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- Data Source
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- KAKEN
- IRDB