| International FP-002 |
| HSV-1 Infection in Trabecular Meshwork Cells and its implications for viral Hypertensive Anterior Uveitis |
| 1 Department of Ophthalmology, College of Medicine, St. Vincent’s Hospital, The Catholic University of Korea
2 Department of Microbiology, College of Medicine, The Catholic University of Korea
3 Personalized Genomic Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology
4 Department of Ophthalmology, College of Medicine, Seoul St. Mary’s Hospital, The Catholic University of Korea |
| Jin A Choi (1), Hyun-hee Ju (1), Ju-Eun Kim(2), Seon-Kyu Kim (3), Donghyun Jee (1), Chan Kee Park (4), Soon-young Paik (2)
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Purpose : Herpes simplex virus type 1 (HSV-1) is causative for hypertensive anterior uveitis. Trabecular meshwork (TM) cells, the key cell type that regulates intraocular pressure (IOP), is considered to be the site of inflammation. We explored the profiles of genes expressed in HSV-1 infected human TM cells.
Methods : Human TM cells were infected with HSV-1 and total RNA was isolated. The global transcriptional gene network analyses were performed in mock-infected and HSV-1 infected TM cells. Ingenuity pathway analysis was used to determine the key biological networks related to the genes that were significantly altered. Quantitative PCR was performed to validate the microarray analyses.
Results : TM cells had a high susceptibility to HSV-1 infection, which was comparable to Vero cells. HSV-1 induced transcriptional suppression of many components related to fibrosis in TM cells. The top biological network related to the genes that were significantly altered upon HSV-1 infection was organismal injury and abnormalities involving TGF-β1 and PDGF-BB. The results of PCR analyses for selected molecules were in good agreement with the microarray data. HSV-1-infected TM cells showed a 20-fold increase in the expression of PDGF-BB, which was further increased by treatment with TGF-β1. HSV-1 also induced a 4-fold increase in the expression of the monocyte chemoattractant protein (MCP)-1, the downstream molecules of PDGF-BB.
Conclusion : In human TM cells, HSV-1 induced transcriptional suppression of many components related to fibrosis and enhanced expression of both PDGF-BB and MCP-1. Our study presented and validated the molecular mechanism during HSV-1 infection in TM cells.
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