March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Altered Retinal Vasculature in Hyperhomocysteinemic Mice
Author Affiliations & Notes
  • Amany M. Tawfik
    Cellular Biology and Anatomy,
    Georgia Health Sciences Univ, Augusta, Georgia
  • Srinivas Sonne
    Biochemistry,
    Georgia Health Sciences Univ, Augusta, Georgia
  • Cory Williams
    Cellular Biology and Anatomy,
    Georgia Health Sciences Univ, Augusta, Georgia
  • Mohamed Al-Shabrawey
    Oral Biology and Anatomy,
    Georgia Health Sciences Univ, Augusta, Georgia
  • Vadivel Ganapathy
    Biochemistry,
    Georgia Health Sciences Univ, Augusta, Georgia
  • Sylvia B. Smith
    Cellular Biology and Anatomy,
    Georgia Health Sciences Univ, Augusta, Georgia
  • Footnotes
    Commercial Relationships  Amany M. Tawfik, None; Srinivas Sonne, None; Cory Williams, None; Mohamed Al-Shabrawey, None; Vadivel Ganapathy, None; Sylvia B. Smith, None
  • Footnotes
    Support  National Eye Institute,NIH Grant EY012830
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 2557. doi:
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      Amany M. Tawfik, Srinivas Sonne, Cory Williams, Mohamed Al-Shabrawey, Vadivel Ganapathy, Sylvia B. Smith; Altered Retinal Vasculature in Hyperhomocysteinemic Mice. Invest. Ophthalmol. Vis. Sci. 2012;53(14):2557.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : Homocysteine (Hcy) is a non-proteinogenic amino acid whose elevation has been implicated in human visual disorders. Recently, we investigated the retinal phenotype of mice with moderate/severe hyperhomocysteinemia due to deficiency/absence, respectively, of the gene encoding cystathionine-beta-synthase (CBS). We reported marked retinal disruption, ganglion cell loss, overstimulation of the NMDA receptor, optic nerve mitochondrial dysfunction and ERG defects in cbs-/- mice and a delayed morphological/functional phenotype in cbs+/- mice (Ganapathy et al, 2009, 2011; Yu et al, 2011). Excess Hcy is an independent risk factor for human systemic cardiovascular diseases such as hypertension; however it is not known whether excess Hcy alters retinal vasculature. We used cbs mutant mice to address this.

Methods: : Retinas of cbs+/+ (n =21), cbs +/- (n = 34), cbs -/- (n =16) mice (age 2 wks) were harvested for wholemount preparation or cryosections and subjected to immunofluorescence microscopy to (1) visualize vessels via the endothelial cell marker isolectin-B4; to detect (2) angiogenesis (VEGF and CD 105 (endoglin)), (3) activated glial cells (GFAP), (4) inflammation (TNF-α) and (5) superoxide production (DHE). Retinal wholemounts were examined by LSCM; cryosections were evaluated using a Zeiss Axioplan-2 microscope and the AxioVision program.

Results: : Retinal vasculature of cbs+/- mice was similar to WT mice, consistent with a normal phenotype at this age (Ganapathy et al, 2009). However, cbs-/- mice demonstrated vascular patterns consistent with ischemia: isolectin B4 labeling revealed a marked capillary-free zone in the central retina and new vessels with capillary tufts in the mid-peripheral area. This altered vascular pattern was associated with increased VEGF and CD105 levels. In retinal cryosections, marked increase in GFAP, consistent with glial cell activation was observed in cbs -/- mice, as were increased levels of TNFα and superoxide.

Conclusions: : The findings suggest that severe elevation of Hcy, as seen in the cbs-/- mouse, is accompanied by alterations in retinal vasculature. The retinal disruption and decreased visual function reported previously in cbs-/- mice may reflect vasculopathy as well as the neuropathy.

Keywords: neovascularization • retina • vascular endothelial growth factor 
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