Journal
MOLECULAR THERAPY-METHODS & CLINICAL DEVELOPMENT
Volume 17, Issue -, Pages 143-155Publisher
CELL PRESS
DOI: 10.1016/j.omtm.2019.11.017
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Funding
- National Natural Science Foundation of China [81770924, 81900829]
- Sanming Project of Medicine in Shenzhen [SZSM201512045]
- Science and Technology Innovation Committee of Shenzhen [GJHZ20170314102535241]
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Glaucoma is a lifelong disease with elevated intraocular pressure (IOP) as the main risk factor, and reduction of IOP remains the major treatment for this disease. However, current IOP-lowering therapies are far from being satisfactory. We have demonstrated that the lentivirus-mediated exoenzyme C3 transferase (C3) expression in rat and monkey eyes induced relatively long-term IOP reduction. We now show that intracameral injection of self-complementary AAV2 containing a C3 gene into mouse and monkey eyes resulted in morphological changes in trabecular meshwork and IOP reduction. The vector-transduced corneal endothelium and the C3 transgene expression, not vector itself, induced corneal edema as a result of actin-associated endothelial barrier disruption. There was a positive (quadratic) correlation between measured IOP and grade of corneal edema. This is the first report of using an AAV to transduce the trabecular meshwork of monkeys with a gene capable of altering cellular structure and physiology, indicating a potential gene therapy for glaucoma.
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