May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
Genetic Networks Modulating Retinal Injury
Author Affiliations & Notes
  • F. Vazquez–Chona
    Ophthalmology, Univ of Tennessee Health Sci Ctr, Memphis, TN
  • E.E. Geisert, Jr.
    Ophthalmology, Univ of Tennessee Health Sci Ctr, Memphis, TN
  • Footnotes
    Commercial Relationships  F. Vazquez–Chona, None; E.E. Geisert, None.
  • Footnotes
    Support  Fight for Sight Student Fellowship (SF04031, FRVC)), RO1EY12369 (EEG), Core Grant 5P30 EY13080; an unrestricted grant from Research to Prevent Blindness
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 5415. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      F. Vazquez–Chona, E.E. Geisert, Jr.; Genetic Networks Modulating Retinal Injury . Invest. Ophthalmol. Vis. Sci. 2006;47(13):5415.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: : Photoreceptor injury and disease activate retinal glial cells. This response is characterized by an increase in soma size, hypertrophy of cellular processes, and proliferation. In specific cases, this remodeling of reactive glial cells creates membranes that can impair photoreceptor survival or retinal healing. Our laboratory is attempting to define master regulators of glial cell remodeling by (1) determining transcriptional changes that underlie glial cell reactivity, and (2) defining networks controlling the early and persistent changes of reactive glia.

Methods: : To define the transcriptional architecture controlling glial cell remodeling, we are analyzing gene expression changes that occur in the injured rat retina with microarray technology, online bioinformatic resources, and computational tools.

Results: : To date, our work has yielded three complementary insights. First, groups of functionally related genes underlie the early, delayed, and sustained responses of reactive glia cells [Vazquez et al., (2004) IOVS]. For example, transcriptional factors such as Stat3 and Nfkb1 defined the early response, whereas, glial reactive markers such as Gfap and Cd81 defined the sustained response. Second, three specific genomic loci modulate coordinate changes in gene expression in mouse CNS [Vazquez et al., (2005) Mol Vis]. Of the three only the regulatory locus on Chromosome 12 specifically modulates the expression of a group of genes involved in early wound–healing events (mainly, the regulation of transcription, differentiation, apoptosis, and proliferation). Third, candidate genes Id2 and Lpin1 are current modulators for the network controlled by the Chromosome 12 locus. Higher levels of Id2 and Lpin1 correlated with higher levels of the survival gene Crygd, and with lower levels of acute phase genes Fos and Stat3, reactive gliosis genes Gfap and Cd81, and apoptotic gene Casp3.

Conclusions: : During this process we developed an integrated approach of gene expression profiling and higher–level bioinformatic analyses to define genetic networks. This work not only advances our understanding of the molecular networks controlling the CNS response to injury, but may also form the basis for interventions that can rescue injured neurons and re–establish lost retinal connections.

Keywords: regeneration • transcription • trauma 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×