研究課題/領域番号 |
22K14548
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研究種目 |
若手研究
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配分区分 | 基金 |
審査区分 |
小区分27040:バイオ機能応用およびバイオプロセス工学関連
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研究機関 | 立命館大学 |
研究代表者 |
ABDALKADER Rodi 立命館大学, 立命館グローバル・イノベーション研究機構, 准教授 (20839964)
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研究期間 (年度) |
2022-04-01 – 2025-03-31
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研究課題ステータス |
交付 (2023年度)
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配分額 *注記 |
4,550千円 (直接経費: 3,500千円、間接経費: 1,050千円)
2023年度: 2,340千円 (直接経費: 1,800千円、間接経費: 540千円)
2022年度: 2,210千円 (直接経費: 1,700千円、間接経費: 510千円)
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キーワード | Cornea-on-a-chip / Microfluidic / Metabolomic / Drug toxicity / cornea-on-a-chip / iPSC / metabolomics |
研究開始時の研究の概要 |
This proposal aims for the development of a dynamic human cornea model in integration with untargeted metabolomics by combining human induced pluripotent stem cells (iPSC), microfluidics technologies, and metabolomics. This approach will allow us to investigate the early toxicity of the ophthalmic drugs through the selection of significant metabolites markers upon drugs exposure.
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研究実績の概要 |
This research aims to identify metabolite markers related to drug toxicity using untargeted metabolomic analysis in a human corneal epithelium-on-a-chip. In the current fiscal year, we successfully investigated the adverse effects of a model drug, diclofenac, a non-steroidal anti-inflammatory drug, in the corneal epithelium-on-a-chip. Through the utilization of untargeted metabolomics and RNA sequencing, we were able to discover metabolite markers and relevant genes associated with diclofenac treatment, such as methyl-2-oxovaleric acid, 3-methyl-2-oxobutanoic acid, and lauroyl-carnitine. This untargeted metabolomic analysis approach in the corneal epithelium-on-a-chip has the potential to be further employed in combination with additional drugs in future.
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現在までの達成度 (区分) |
現在までの達成度 (区分)
1: 当初の計画以上に進展している
理由
The advancement of this research can be credited to the effective implementation of an optimized untargeted metabolomic method for detecting extracellular metabolites in a corneal epithelium-on-a-chip model. Additionally, the capability to validate the system with a drug model has facilitated the discovery of new metabolite markers.
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今後の研究の推進方策 |
Based on current progress, we will initially investigate the function of the discovered metabolite markers to determine if they serve as toxic markers when tested with a larger set of drugs. Secondly, we will explore the sensitivity of these markers by examining their correlation with the early onset of relevant gene expression. Additionally, we will concentrate on employing human cells derived from human induced pluripotent stem cells (iPSCs).
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