Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.23 (beta-galactosidase)
 14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic retinopathy is a major cause of acquired blindness due to the development of retinal neovascularization and associated traction retinal detachment. It is commonly treated with retinal photocoagulation therapy; however, progression to blindness remains a significant problem. To determine the feasibility of adjunctive anti-angiogenic gene therapy, we evaluated the capability of retroviral vectors, which transfer exogenous genes only into dividing cells, to transfer and express a beta-galactosidase gene selectively into photocoagulation sites. Thirty-five rabbits received 30 retinal photocoagulation burns in the right eye followed 2 days later by beta-galactosidase (G1nBgSvNa) or control (G1XSvNa) vector injection into the subretinal space. Beta-galactosidase expression was observed in the photocoagulation sites from 5 days after vector administration (31.7+/-7.0%) to 12 weeks (6.7+/-3.4%). Immunohistochemical studies of the treated retinas using antibody Ber-MAC3 and anti-cytokeratin antibodies revealed that transduced cells were macrophages and retinal pigment epithelial cells. To determine feasibility in a primate, two monkeys received 10 laser burns in the macula superior to the fovea followed 2 days later by G1nBgSvNa vector. beta-galactosidase expression was found in photocoagulation sites and foveal retina was well preserved. We conclude that gene transfer to retinal photocoagulation sites provides stable expression of the transduced gene with relatively high efficiency. This feasibility study suggests the possibility of transferring genes encoding for anti-angiogenic factors into photocoagulation sites to improve the efficacy of laser photocoagulation therapy.
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PMID:Retrovirus-mediated gene transfer targeted to retinal photocoagulation sites. 962 65

This study was conducted to investigate a method of gene therapy for proliferative vitreoretinopathy (PVR) by inhibiting type beta transforming growth factor (TGF-beta). PVR was induced in pigmented rabbits by intravitreal injection of 50 000 rabbit conjunctival fibroblasts after vitrectomy. Subsequently, the eyes received an intravitreal application of adenovirus vector encoding a soluble type II TGF-beta receptor (AdTbeta-ExR, n = 10) or adenoviral vector expressing beta-galactosidase (AdLacZ) (n = 10) or balanced salt solution (BSS) (n = 6). The eyes were examined ophthalmoscopically for 28 days after surgery, and the clinical stage of PVR was evaluated on a scale of zero to five. Histological examinations were performed on the treated eyes on day 28. All control eyes injected with AdLacZ or BSS developed PVR, characterized by retinal detachment and the formation of intravitreal membranes within 7 days. The eyes injected with AdTbeta-ExR also developed features of PVR, but the average severity from day 5 to day 28 was significant lower than in the control eyes (P < 0.05). TGF-beta plays an important role in PVR progression in a PVR model, and prevention of TGF-beta signaling could be therapeutically useful.
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PMID:Gene transfer of soluble TGF-beta type II receptor inhibits experimental proliferative vitreoretinopathy. 1221 88