| Budget Amount *help |
¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2019: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Outline of Final Research Achievements |
We have established a new hypothesis that epithelial-mesenchymal transition (EMT)-like changes in trabecular meshwork cells contribute to glaucoma pathology. The purpose of this study was development of new therapeutic methods based on the plasticity of cells. Trabecular meshwork cells showed EMT-like changes such as extracellular matrix production enhancement, F-actin increase and α-SMA expression enhancement upon TGF-β2 stimulation. The HDAC inhibitor vorinostat significantly suppressed these EMT-like changes. Furthermore, vorinostat significantly suppressed the increase of aqueous humor outflow resistance induced by TGF-β2 stimulation in perfusion experiments. Thus, the HDAC inhibitor vorinostat was shown to suppress the increase in aqueous humor outflow resistance induced by TGF-β2.
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