May 2007
Volume 48, Issue 13
ARVO Annual Meeting Abstract  |   May 2007
Muller Glial Cell Response to Retina Degeneration
Author Affiliations & Notes
  • K. Roesch
    Genetics, Harvard Medical School, Boston, Massachusetts
  • A. Jadhav
    Genetics, Harvard Medical School, Boston, Massachusetts
  • C. Punzo
    Genetics, Harvard Medical School, Boston, Massachusetts
  • B. Sun
    Genetics, Harvard Medical School, Boston, Massachusetts
  • C. Cepko
    Genetics, Harvard Medical School, Boston, Massachusetts
  • Footnotes
    Commercial Relationships K. Roesch, None; A. Jadhav, None; C. Punzo, None; B. Sun, None; C. Cepko, None.
  • Footnotes
    Support National Eye Institute Grant R01 EY014466
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 2948. doi:
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      K. Roesch, A. Jadhav, C. Punzo, B. Sun, C. Cepko; Muller Glial Cell Response to Retina Degeneration. Invest. Ophthalmol. Vis. Sci. 2007;48(13):2948.

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

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Purpose:: Neuronal cell death in the CNS often involves changes in non-neuronal cells. This holds for rod photoreceptor death in the murine retina. Resident Muller glial cells, the major type of glia in the mammalian retina, have been shown to respond to neuronal cell death by increasing GFAP expression. In order to identify the molecular machinery that defines Muller glial cell identity and function, single cell gene expression profiling was performed. A model of retinitis pigmentosa (RP), in which the rhodopsin gene is deleted, was used for the study of Muller glial response to rod photoreceptor degeneration.

Methods:: Single cell gene profiling of Muller glia was achieved using Affymetrix arrays and validated by in situ hybridization on retinal sections.

Results:: Profiling of Muller glia from wild type and rhodopsin -/- mice led to the identification of a cluster of genes expressed at high levels in Muller glial cells, including transcripts that were not previously characterized in (Muller) glia. These genes likely contribute to many of the functions of Muller glia. Validation of the expression of many of these genes was performed by in situ hybridization. Distinct clusters of differentially expressed genes were observed in retinae of the rhodopsin-/- mice.

Conclusions:: These data establish the molecular fingerprint of Muller glia and provide a foundation for further studies of Muller glia development and function in normal and diseased states.

Keywords: Muller cells • retinal degenerations: cell biology • gene microarray 

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