June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Modulation of Retinal Neovascularization with Novel Related Transcriptional Enhancer Factor-1 (RTEF1 or TEAD4) Isoforms
Author Affiliations & Notes
  • Tawfik Issa
    Cullen Eye Institute, Houston, TX
  • Matthew Hartzell
    Cullen Eye Institute, Houston, TX
  • Tim Stout
    Cullen Eye Institute, Houston, TX
  • Footnotes
    Commercial Relationships Tawfik Issa, None; Matthew Hartzell, None; Tim Stout, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 2315. doi:
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      Tawfik Issa, Matthew Hartzell, Tim Stout; Modulation of Retinal Neovascularization with Novel Related Transcriptional Enhancer Factor-1 (RTEF1 or TEAD4) Isoforms. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):2315.

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

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Abstract

Purpose: Wet AMD and diabetic retinopathy are diseases that are associated with retinal neovascularization and may lead to blindness. Increased expression of vascular endothelial growth factor (VEGF) has been correlated with the development of retinal neovascularization in both diseases. We have previously demonstrated a role for RTEF isoforms in the control of VEGF expression. We previously identified two related transcriptional enhancer factor-1 isoforms (TEAD4216 and TEAD4148). The TEAD4216 isoform represses VEGF expression while the TEAD4148 isoform enhances VEGF expression in mammalian cells.<br /> We have generated transgenic mice on C57BL/6J background which overexpress the TEAD4216 or TEAD4148 isoforms.<br /> In this report we evaluate the effect of the transgene on the developmental retinal angiogenesis.

Methods: Retinal flat mounts from adult transgenic mice and age matched wild-type control were prepared and stained with isolectin. The vascular network was examined via fluorescent microscopy.

Results: We performed a qualitative assessment of the retinal vasculature on retinal flat-mount. Retinas from normal wild-type mice exhibited normal superficial vascularization which extended from the optic nerve to the periphery. Retinas from TEAD4216 and TEAD4148 transgenic mice had perturbed microvascularization.

Conclusions: These findings indicate that TEAD4216 and TEAD4148 may influence normal retinal vascularization.<br /> Additional TEAD4216 and TEAD4148 mice will need to be examined in the future to determine the effect of the transgene on non-ocular vascular development and the development of hyperoxic retinopathy

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