Roles of miR-100 in endometriosis
| Project/Area Number |
16K11093
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Oita University |
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Principal Investigator |
Nasu Kaei 大分大学, 医学部, 教授 (30274757)
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| Co-Investigator(Kenkyū-buntansha) |
平川 東望子 大分大学, 医学部, 客員研究員 (20516132)
河野 康志 大分大学, 医学部, 准教授 (40274758)
楢原 久司 大分大学, 医学部, 教授 (60211447)
西田 正和 大分大学, 医学部, 講師 (90404384)
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| Project Period (FY) |
2016-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2018: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2017: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 子宮内膜症 / マイクロRNA / 遊走能 / 浸潤能 / エピジェネティクス / SMARCD1 / MMP1 / 形質獲得 / 病態 / マイクロアレイ |
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| Outline of Final Research Achievements |
The present study aimed to elucidate the roles of has-miR-100-5p in the pathogenesis of endometriosis. Normal endometrial stromal cells (NESCs) were isolated from normal eutopic endometrium without endometriosis. Using hsa-miR-100-5p-transfected NESCs, we evaluated the effect of hsa-miR-100-5p on the invasiveness of these cells by Transwell invasion assay and in-vitro wound repair assay. We also investigated the downstream signal pathways of hsa-miR-100-5p by microarray analysis and Ingenuity pathways analysis.
hsa-miR-100-5p transfection enhanced the invasion and motility of NESCs. After hsa-miR-100-5p transfection, mRNA expression of SMARCD1 was significantly attenuated whereas, the expression of MMP1 mRNA and active MMP1 protein levels was upregulated.
These findings suggest that enhanced hsa-miR-100-5p expression in endometriosis is involved in promoting the acquisition of endometriosis-specific characteristics during endometriosis development.
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| Academic Significance and Societal Importance of the Research Achievements |
子宮内膜症の原因解明を目的として、マイクロRNAの発現異常に着目し、エピジェネティクスの観点から検討を行った。本研究では、卵巣子宮内膜症性嚢胞間質細胞において発現が亢進しているmiR-100が子宮内膜症の病態形成に関与することが明らかとなった。
子宮内膜症は年々増加しており、比較的若年層の女性に好発することから、注目度の高い疾患である。本研究の成果は、子宮内膜症の病態解明と新規薬物療法の開発に寄与するものと考えられる。
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Report
(6 results)
Research Products
(51 results)
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[Journal Article] miR-503, a microRNA epigenetically repressed in endometriosis, induces apoptosis and cell-cycle arrest and inhibits cell proliferation, angiogenesis, and contractility of human ovarian endometriotic stromal cells.2016
Author(s)
Hirakawa T, Nasu K, Abe W, Aoyagi Y, Okamoto M, Kai K, Takebayashi K, Narahara H.
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Journal Title
Human Reproduction
Volume: 31
Issue: 11
Pages: 2587-2597
DOI
Related Report
Peer Reviewed / Acknowledgement Compliant
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