| Project/Area Number |
18K15982
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 53040:Nephrology-related
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| Research Institution | Kagoshima University |
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Principal Investigator |
Miyazono Akinori 鹿児島大学, 医歯学域鹿児島大学病院, 助教 (10795503)
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| Project Period (FY) |
2018-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | ネフローゼ症候群 / 血小板 / microRNA / 足細胞 / miR-223 / microRNA 223 / VEGF-A |
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| Outline of Final Research Achievements |
I made a nephrotic model by administering puromycin aminonucleoside intravenously to 6-week-old SD rats. When a suspension of Exosome enriched with miR-223 derived from human megakaryoblastic leukemia cell Meg-01 was administered intravenously, urine protein/Cr was higher than that of the intravenous normal saline group.
I attempted to create a glomerular model using murine glomerular endothelial cells and podocytes. Podocytes were treated according to the product sheet. It was stated that podocytes were induced to differentiate when incubated at 38°C and stopped growing after 2 to 4 weeks, but no differentiation could be induced after 4 weeks. Protein and mRNA were extracted from podocytes and analyzed by Western-Blotting and RT-PCR, but no nephrin or synaptopodin, proteins specific to podocyte, were detected. The acquired cells themselves were thought to lack the character of a podocyte.
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| Academic Significance and Societal Importance of the Research Achievements |
小児のネフローゼ症候群(NS)は大部分が原因不明である。難治例では長期のステロイド治療を余儀なくされ、成長障害や肥満、精神症状などの副作用に苛まれる。NSでは血小板の数や形態の異常を合併することが知られる。NSを模したラットに血小板由来のmicroRNAを注射するとNSの病勢は悪化したことからは、血小板に含有されるmicroRNAがNSの病態に関わっていることが伺えた。血小板に着目して診療することで、NSの病勢予測や治療方針の決定につながる可能性があり、究極的にはNSの発症要因にもつながると考えている。
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