April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Conditional Smad7 Knockdown Causes Elevated Number Of Müller Glia And Increased Nestin Expression In The Central Retina
Martina Klupp; Rudolf Fuchshofer; Barbara Braunger; Ernst R. Tamm; Ludwig Aigner
Author Affiliations & Notes
  • Martina Klupp
    Institute of Human Anatomy and Embryology, University of Regensburg, Regensburg, Germany
    Institute of Molecular Regenerative Medicine, Paracelsus Medical University, Salzburg, Austria
  • Rudolf Fuchshofer
    Institute of Human Anatomy and Embryology, University of Regensburg, Regensburg, Germany
  • Barbara Braunger
    Institute of Human Anatomy and Embryology, University of Regensburg, Regensburg, Germany
  • Ernst R. Tamm
    Institute of Human Anatomy and Embryology, University of Regensburg, Regensburg, Germany
  • Ludwig Aigner
    Institute of Molecular Regenerative Medicine, Paracelsus Medical University, Salzburg, Austria
  • Footnotes
    Commercial Relationships  Martina Klupp, None; Rudolf Fuchshofer, None; Barbara Braunger, None; Ernst R. Tamm, None; Ludwig Aigner, None
  • Footnotes
    Support  Supported by DFG Research Unit FOR 1075
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 913. doi:
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      Martina Klupp, Rudolf Fuchshofer, Barbara Braunger, Ernst R. Tamm, Ludwig Aigner; Conditional Smad7 Knockdown Causes Elevated Number Of Müller Glia And Increased Nestin Expression In The Central Retina. Invest. Ophthalmol. Vis. Sci. 2011;52(14):913.

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Abstract

Purpose: : To investigate the effects of TGF-beta signaling on Müller cell development, we studied mice with a conditional knockout of Smad7, an endogenous inhibitor of TGF-beta signaling. There is evidence that Müller cells have the potential to act as progenitor cells upon injury. As Müller cells are not able to proliferate under physiological conditions, and TGF-beta is known to impair proliferation of progenitor cells (Wachs et al. 2006) in the brain, we hypothesized that proliferation of Müller cells in the retina is under the influence of TGF-beta signaling.

Methods: : Floxed Smad7 mice, with LoxP sites flanking exon 1 of the Smad7 gene, were crossed with EIIa-Cre mice to generate heterozygous Smad7-deficient animals. Decreased expression of Smad7 was confirmed by quantitative real-time PCR. Thickness of the retina was measured on semithin sections at postnatal day (P) 20. Müller cells at P20 were stained with an antibody against glutaminsynthetase on frozen sections and counted in the central, medial and peripheral retina. In addition, nestin staining as an indicator of Müller cell activation was performed on frozen sections at P20. For statistical analysis, a student’s t-test was performed(p < 0.05).

Results: : Heterozygous Smad7-deficient mice showed a significantly thickened central retina (p < 0.03) and a significantly thickened inner nuclear layer (p < 0.02) at the optic nerve head. In addition, heterozygous Smad7-deficient mice also showed significantly more Müller glia than their wildtype littermates in the central retina (p < 0.05). Furthermore, an enhanced immunoreactivity for nestin was observed in Müller cells of the central and medial retina.

Conclusions: : We suppose that the reduced expression of Smad7 in heterozygous Smad7-deficient animals and the resulting increase in TGF-beta signaling leads to an elevated number of Müller cells during development. Whether these effects are due to an increase in proliferation or a protection against apoptosis needs to be shown.

Keywords: Muller cells • retina • glia 
© 2011, The Association for Research in Vision and Ophthalmology, Inc., all rights reserved. Permission to republish any abstract or part of an abstract in any form must be obtained in writing from the ARVO Office prior to publication.
Copyright © 2024 Association for Research in Vision and Ophthalmology.
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