| CR F-001 |
| Reduced NGF level promotes Epithelial-Mesenchymal Transition in dexamethasone treated-human lens epithelial cells via Akt pathway |
| Gyeongsang National University, Department of ophthalmology¹, Gyeongsang National University Hospital, Clinical Research Institute² |
| Yu-Jin, Choi1, Woong-Sun, Yoo1, Young-Sool, Hah2, Hyun A, Kim1, Min-Ho, Shin1, Inyoung, Chung1, Seong-Jae, Kim1 |
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목적 : The effect of NGF on human lens epithelial cells (HLECs) and its regulatory mechanism have not previously been reported. In the present study, we investigated the possible molecular mechanisms underlying the protective effects of NGF against steroid-induced cataract formation in dexamethasone (DEX)-treated HLEC.
방법 : Human lens epithelial B-3 (HLE-B3) cell were treated with DEX, and then cell viability was assessed by using the Cell Counting Kit-8 (CCK-8) assay. Gene expression level of NGF, fibronectin, α-smooth muscle actin (α-SMA), and E-cadherin were measured by real-time quantitative polymerase chain reaction (qPCR). Protein levels of NGF, fibronectin, α-SMA, E-cadherin, Tropomyosin receptor kinase A (TrkA), and Akt were measured by Western blot analysis. PCR array was used to profile gene expression of growth factors in DEX-treated HLECs.
결과 : Increased EMT marker expression and migration activity were found, while the expression of NGF markedly downregulated, in DEX-treated HLE-B3 cells. Increased expression of α-SMA and fibronectin and cell proliferation could be significantly attenuated by NGF treatment. We found that the decreased activation of Akt induced by DEX treatment was significantly recovered by NGF treatment in HLECs.
결론 : This study demonstrates that NGF/TrkA can repress EMT though its targeting of Akt pathway in DEX treated HLECs and NGF might be a novel therapeutic target for steroid-induced cataract.
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