2017 Fiscal Year Final Research Report
Search for unknown endogenous NOD1 ligands acting in the early stage of atherosclerosis
Project/Area Number |
16K19651
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Pediatrics
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Research Institution | Kyushu University |
Principal Investigator |
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Project Period (FY) |
2016-04-01 – 2018-03-31
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Keywords | NOD1 / 動脈硬化 / 自然免疫 |
Outline of Final Research Achievements |
Nucleotide-binding oligomerization domain (NOD)-1, which is an innate immune receptor recognizing bacterial peptidoglycan fragments, contributes to the development of atherosclerosis from early stage. Under germ-free condition, we analyzed the effect of Nod1 deficiency on the development of atherosclerosis in Apoe-/- mice. Nod1 deficiency resulted in reduced development of atherosclerotic lesions in Apoe-/- mice even without a microbiota. This result suggests the contribution of endogenous Nod1 ligands to the development of atherosclerosis. But we failed to determine the NOD1-stimulatory activity of mice atherosclerotic plaque by a bioassay using NOD1-expressing HEK293 cells, suggesting that the Nod1-stimulatory activity of Apoe-/- mice plaque might be very low.
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Free Research Field |
感染免疫
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