2022 Fiscal Year Final Research Report
Involvement of Cdk5 and the ERK pathway in proliferative diabetic retinopathy
Project/Area Number |
20K18345
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Research Category |
Grant-in-Aid for Early-Career Scientists
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Allocation Type | Multi-year Fund |
Review Section |
Basic Section 56060:Ophthalmology-related
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Research Institution | The University of Tokushima |
Principal Investigator |
NIKI Masanori 徳島大学, 大学院医歯薬学研究部(医学域), 助教 (20861082)
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Project Period (FY) |
2020-04-01 – 2023-03-31
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Keywords | 外科 |
Outline of Final Research Achievements |
PPARγ, Cdk5 and p35 concentrations in the vitreous body were significantly higher in the PDR group compared with the control group. Phosphorylated ERK concentration was also higher in the PDR group compared with the control group, but the difference was not significant. Furthermore, the messenger ribonucleic acid expression levels of PPARγ, Cdk5 and p35 in proliferative neovascular membranes were significantly higher in the PDR group compared with the control group. That level of phosphorylated ERK was also higher in the PDR group compared with the control group, but the difference was not significant. Immunostaining showed increased protein expression levels of PPARγ,Cdk5 and p35 in proliferative neovascular membranes in the PDR group compared with the control group.
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Free Research Field |
眼科
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Academic Significance and Societal Importance of the Research Achievements |
PPARγ、Cdk5 とその活性化サブユニットであるp35の眼内濃度は、PDR群において有意に増加していた。さらに、増殖膜におけるPPARγ、Cdk5、p35のmRNAの発現は、PDR群において対照群よりも有意に高く、PDR群の増殖膜での免疫染色では、これらの蛋白の発現の増加が見られた。 以上のことから、Cdk5の活性化はPPARγの発現を介した血管新生等のPDRの病因に関与している可能性がある。各因子の相関をさらに研究することにより、Cdk5を介したPPARγのリン酸化の阻害が、PDRの治療のための新しい治療標的になり得ると考える。
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