April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Adenovirus-Mediated Brain-Derived Neurotropic Factor Protecting RGCs Injury Induced by the Chronic Ocular Hypertension in Rats
Author Affiliations & Notes
  • J. Wang
    Glaucoma,
    Tianjin Medical University Eye Center, Tianjin, China
  • X. Li
    Retina,
    Tianjin Medical University Eye Center, Tianjin, China
  • J. Ge
    Glaucoma, Zhongshan Ophthalmic Center, Guangzhou, China
  • T. T. Lam
    Toxicology, Covance Laboratories, Madison, Wisconsin
  • A. A. Sadun
    Neuro-Ophthal/Keck-USC Sch of Med, Doheny Eye Institute, Los Angeles, California
  • Footnotes
    Commercial Relationships  J. Wang, None; X. Li, None; J. Ge, None; T.T. Lam, None; A.A. Sadun, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 3172. doi:
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      J. Wang, X. Li, J. Ge, T. T. Lam, A. A. Sadun; Adenovirus-Mediated Brain-Derived Neurotropic Factor Protecting RGCs Injury Induced by the Chronic Ocular Hypertension in Rats. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3172.

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Abstract

Purpose: : To investigate the protection of adenoassociated virus (AAV)-mediated brain-derived neurotrophic factor (BDNF) to RGCs injured by the chronic ocular hypertension in rat.

Methods: : AAV-BDNF and AAV-GFP vector were constructed. The rats were randomly divided into experimental group (n = 36) and the control group (n = 36). The rats in experimental group were injected to the vitreous chamber with 2µl AAV-BDNF vector, and the sham injection with 2µl AAV-GFP vector. The RGCs were retrograde labeled by fluorogold in one week later, after 2 weeks the rat model of chronic ocular hypertension was established. At 8 weeks, the animals were sacrificed and the eyes were enucleated for the flatmounted retinas counting RGCs (n = 9), immunofluorescence staining, western blot and real time RT PCR (n=9), as well as untra-thin sections of optic nerve for PPD staining (n=9).

Results: : The number of RGCs in experimental group was 2465 ± 249 and that in control group was 1753 ± 211, which was significant difference (P<0.05). Thy-1 (marker of RGCs) staining showed the RGCs loss was detected in control group. The mRNA and protein expression of Thy-1, Brn-3a, NF-L increased significantly in AAV-BDNF group comparing with AAV-GFP group (P<0.05). PPD staining showed that optic nerve axons were damaged significantly in control group.

Conclusions: : AAV-BDNF plays a protective role in RGCs injury induced by the chronic ocular hypertension in rat, gene therapy may become a new means of treating glaucoma.

Keywords: neuroprotection 
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