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Your search keyword '"glaucoma filtration surgery (GFS)"' showing total 2 results
Start Over Descriptor "glaucoma filtration surgery (GFS)" Publisher impact journals, llc
2 results on '"glaucoma filtration surgery (GFS)"'

1. The TβR II-targeted aptamer S58 prevents fibrosis after glaucoma filtration surgery

Author

Ziwen Wang, Zujuan Liu, Lin Xie, Chongxing Shen, Xiangji Li, Yu Leng, Peng Luo, Yawei Wang, Xueru Li, Chi Zhang, Long Chen, Xiaofeng Yue, and Chunmeng Shi

Subjects
Aging, Intraocular pressure, NF-E2-Related Factor 2, Glaucoma, Pharmacology, glaucoma filtration surgery (GFS), Fibrosis, Nrf2/PI3k/Akt, medicine, Animals, Humans, Bleb (cell biology), Protein kinase B, Cells, Cultured, PI3K/AKT/mTOR pathway, business.industry, fibrosis, Receptor, Transforming Growth Factor-beta Type II, aptamer, S58, Cell Biology, Aptamers, Nucleotide, Fibroblasts, medicine.disease, In vitro, Disease Models, Animal, Oxidative Stress, Filtering Surgery, Rabbits, business, Conjunctiva, Intracellular, Research Paper
Abstract

Glaucoma filtration surgery (GFS) is an effective clinical treatment for glaucoma when intraocular pressure (IOP) control is poor. However, the occurrence of conjunctival scarring at the surgical site is the main reason for failure of the surgery. In a previous study, we isolated and developed S58, a novel nucleic acid aptamer targeting TβR II, by systematic evolution of ligands by exponential enrichment (SELEX). Here, we show how S58 sterically inhibits the TβR II interaction with TGF-β. The effects of topical S58 treatment were studied in a rabbit model of GFS. At 6 postoperative weeks, S58 reduced fibrosis and prolonged bleb survival in rabbits after GFS. Further in vitro tests showed that the levels of fibrosis in S58 treated-Human Conjunctival Fibroblasts (HConFs) were decreased and that antioxidant defense was increased. In addition, the loss of nuclear factor erythroid 2-related factor 2 (Nrf2) or the inhibition of phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) reversed the anti-fibrotic effects of S58. The present work suggests that S58 could effectively improve GFS surgical outcomes by activating the intracellular antioxidant defense PI3K/Akt/Nrf2 signaling pathway.

Published
2020
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2. The TβR II-targeted aptamer S58 prevents fibrosis after glaucoma filtration surgery.

Author

Li X, Leng Y, Li X, Wang Y, Luo P, Zhang C, Wang Z, Yue X, Shen C, Chen L, Liu Z, Shi C, and Xie L

Subjects
Animals, Cells, Cultured, Conjunctiva cytology, Disease Models, Animal, Fibroblasts drug effects, Glaucoma surgery, Humans, NF-E2-Related Factor 2 metabolism, Oxidative Stress drug effects, Rabbits, Aptamers, Nucleotide metabolism, Aptamers, Nucleotide pharmacology, Fibrosis etiology, Fibrosis metabolism, Fibrosis prevention & control, Filtering Surgery adverse effects, Receptor, Transforming Growth Factor-beta Type II metabolism
Abstract

Glaucoma filtration surgery (GFS) is an effective clinical treatment for glaucoma when intraocular pressure (IOP) control is poor. However, the occurrence of conjunctival scarring at the surgical site is the main reason for failure of the surgery. In a previous study, we isolated and developed S58, a novel nucleic acid aptamer targeting TβR II, by systematic evolution of ligands by exponential enrichment (SELEX). Here, we show how S58 sterically inhibits the TβR II interaction with TGF-β. The effects of topical S58 treatment were studied in a rabbit model of GFS. At 6 postoperative weeks, S58 reduced fibrosis and prolonged bleb survival in rabbits after GFS. Further in vitro tests showed that the levels of fibrosis in S58 treated-Human Conjunctival Fibroblasts (HConFs) were decreased and that antioxidant defense was increased. In addition, the loss of nuclear factor erythroid 2-related factor 2 (Nrf2) or the inhibition of phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) reversed the anti-fibrotic effects of S58. The present work suggests that S58 could effectively improve GFS surgical outcomes by activating the intracellular antioxidant defense PI3K/Akt/Nrf2 signaling pathway.

Published
2020
Full Text
View/download PDF

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