2021 Fiscal Year Final Research Report
Inhibitory Effects of Decorin on Epithelial-mesenchymal transition in the Lens and Its Effects on Lens Regeneration
| Project/Area Number |
19K18860
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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 56060:Ophthalmology-related
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| Research Institution | Kanazawa Medical University |
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Principal Investigator |
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| Project Period (FY) |
2019-04-01 – 2022-03-31
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| Keywords | デコリン / 水晶体 / 後発白内障 / 水晶体再生 / 上皮間葉系移行 |
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| Outline of Final Research Achievements |
The expression of Decorin（DCN） was significantly upregulated in rat PCO tissues compared to that observed in the control using a microarray-based approach. LECs treated with fibroblast growth factor (FGF) 2 displayed an enhanced level of DCN expression, while LECs treated with transforming growth factor (TGF)β-2 showed a decrease in DCN expression. No phenotypic changes were observed in the lenses of 8- and 48-week-old transgenic mice for lens-specific hDCN (hDCN-Tg). Injury-induced EMT of the mouse lens, and the expression patterns of α smooth muscle actin, were attenuated in hDCN-Tg mice lenses. Overexpression of DCN inhibited the TGFβ-2-induced upregulation of Tpm1 and EMT observed during wound healing of the lens, but it did not affect mouse lens morphology until 48 weeks of age.
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| Free Research Field |
後発白内障
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| Academic Significance and Societal Importance of the Research Achievements |
我々は，Rat PCO組織のマイクロアレイを用いた網羅的な解析にて、デコリン(Dcn)が上昇し、水晶体の創傷治癒を促進させて線維化を抑制することを国内外で初めて報告した。
DCNはヒト房水に分泌されているタンパク質であり、眼内での毒性もない。分泌タンパク質DCNが、EMTを抑制していることが今回の研究で解明され、DCNはEMTが関連する眼疾患(後発白内障や増殖硝子体網膜症など)を抑制する新しい治療薬のターゲットとなる可能性が示唆された。
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