Analysis of pain mechanism focused on prostaglandin I2 during orthodontic tooth movement
Project/Area Number |
16H06818
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Research Category |
Grant-in-Aid for Research Activity Start-up
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Allocation Type | Single-year Grants |
Research Field |
Orthodontics/Pediatric dentistry
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Research Institution | Niigata University |
Principal Investigator |
Ohkura Mariko 新潟大学, 医歯学総合病院, 医員 (50779634)
|
Project Period (FY) |
2016-08-26 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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Keywords | プロスタグランジンI2 / TRPV1 / 矯正 / 疼痛 / IP受容体 / PGIS / IP |
Outline of Final Research Achievements |
This study attempted to analyze the mRNA and protein expression of prostaglandin I2 synthase, IP receptor, and TRPV1 with real-time PCR and immunohistostaining in experimental force-applied rat molar pulp tissue. PGIS was immunolocalized in odontoblasts and some fibroblasts in the forced-stimulated pulp. The IP receptor and TRPV1 were detected on odontoblasts and some neuron fibers. It was conclude that PGIS, IP receptor, and TRPV1 in rat molar pulp were significantly upregulated shortly after the force application, and that the IP receptor was co-expressed on TRPV1 expressing nerves and odontoblasts. These findings suggest that the PGI2-IP receptor-TRPV1 pathway is associated with the acute phase of force induced pulp changes involving odontoblasts and nerves.
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Report
(3 results)
Research Products
(4 results)