December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
NFkB Essential Modulator (NEMO) is Inducible by Hypoxia and May Play a Role in Retinal Neovascularization
Author Affiliations & Notes
  • JA Pearlman
    Chief Resident's Office Wilmer Eye Institute B-20 Baltimore MD
  • Footnotes
    Commercial Relationships   J.A. Pearlman, None. Grant Identification: Education grant from Pharmacia/Upjohn
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 4019. doi:
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      JA Pearlman; NFkB Essential Modulator (NEMO) is Inducible by Hypoxia and May Play a Role in Retinal Neovascularization . Invest. Ophthalmol. Vis. Sci. 2002;43(13):4019.

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

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Abstract: : Purpose: NFkB essential modulator (NEMO) is involved in the pathogenesis of incontinentia pigmenti, an X-linked dominant disorder resulting in dermatologic, dental, ocular and neurologic defects. NEMO controls the activity of NFkB, a key regulator of cell proliferation, survival, and the stress response. As some patients develop peripheral retinal neovascularization, we sought to determine whether NEMO was inducible by hypoxia, hypothesizing that it may be an angiogenic factor in the retina. Methods: Oligonucleotides specific for murine NEMO as well as controls (the Von-Hippel Lindau gene [VHL], vascular endothelial growth factor [VEGF], and hypoxia-inducible factor 1 [HIF-1]) were synthesized. Newborn C57Bl/10 mice were exposed to 78% oxygen from postnatal day 7 to 12, then returned to room air, inducing the development of retinal neovascularization. Age-matched control animals were kept at room air through post-natal day 14. The eyes were enucleated on postnatal day 14, and RNA isolated. Semiquantitative RT-PCR was performed to assess the relative levels of each transcript in the eyes. Results: As expected, the HIF-1 and VEGF transcripts were upregulated by hypoxia. The NEMO transcript was also upregulated in a similar fashion. The VHL transcript was unaffected. Conclusion: NEMO, a key regulator of NFkB and the genetic defect in incontinentia pigmenti, is regulated by hypoxia and may be an angiogenic factor in the retina. Moreover, it may serve as a target for novel antiangiogenic therapies.

Keywords: 566 retinal neovascularization • 417 gene/expression • 316 animal model 

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