Plasma RNA induces inflammatory response of preeclampsia via TLR3 activation.
| Project/Area Number |
25861469
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Chiba University |
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Principal Investigator |
NAKADA Emiri 千葉大学, 医学部附属病院, 助教 (30447289)
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| Project Period (FY) |
2015-03-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 妊娠高血圧症候群 / TLR3 / ＴＬＲ３ |
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| Outline of Final Research Achievements |
Toll-like receptor (TLR)-mediated inflammation is believed to be of critical importance not only in systemic infectious diseases but also in non-infectious auto-immune disorders. Preeclampsia is characterized by a systemic inflammatory response. TLRs are known to bind to pathogen-associated molecular patterns expressed by microorganisms and endogenous molecules.
We tested the hypothesis that plasma-derived mRNA in preeclampsia induces an inflammatory response in a trophoblast cell via TLR3 and pathogenesis of Preeclampsia. We found trophoblast cells respond to TLR3 stimulation with plasma-derived RNA resulting in expression of inflammatory mediators. Preeclamptic plasma derived RNA signals induced a higher inflammatory response via TLR3. The lipid encapsulated RNA that is observed in the blood of patients with Preeclampsia may be an important endogenous ligand for TLR3. TLR3 ligation then may contribute to the inflammatory response that defines preeclampsia.
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Report
(3 results)
Research Products
(1 results)
