2010 Fiscal Year Final Research Report
The treatments of proliferative vitreoretinopathy by inhibition of TGF-b signaling
| Project/Area Number |
20592050
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | Oita University |
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Principal Investigator |
KIMOTO Kenichi Oita University, 医学部, 講師 (50315339)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIOKA Hidekatsu 大分大学, 医学部, 教授 (00222430)
MATSUO Noritaka 大分大学, 医学部, 准教授 (10284788)
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| Project Period (FY) |
2008 – 2010
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| Keywords | 眼細胞生物学 / 網膜色素上皮 / 増殖性硝子体網膜症 / コラーゲン / シグナル伝達 / TGF-β |
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| Research Abstract |
Transforming growth factor (TGF)-β is a key mediator of proliferative vitreoretinopathy, but the cellular mechanisms by which TGF-β induces extracellular matrix protein (ECM) synthesis are not fully understood. This study examined whether the PI3K/Akt pathway is involved in TGF-β2-induced collagen expression in human retinal pigment epithelial cells. The biochemical blockade of PI3K/Akt activation inhibited TGF-β2-induced type I collagen mRNA expression and type I collagen synthesis. The blockade of PI3K/Akt pathway inhibited the increase in COL1A2 promoter activities when induced by TGF-β2 and reduced TGF-β2 induction of Smad-mut/Luc promoter activity and CAGA12-Luc activity. Moreover, wortmannin increased the TGF-β2-induced Smad7 mRNA expression levels. The PI3K/Akt pathway plays a role in relaying the TGF-β2 signal to induce type I collagen synthesis in the retinal pigment epithelium through Smad-dependent and Smad-independent pathway.
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