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Misexpression of IGF-I in the mouse lens expands the transitional zone and perturbs lens polarization

Academic Article
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Overview

authors

  • Shirke, S.
  • Faber, S. C.
  • Hallem, E.
  • Makarenkova, Helen
  • Robinson, M. L.
  • Overbeek, P. A.
  • Lang, R. A.

publication date

  • March 2001

journal

  • Mechanisms of Development  Journal

abstract

  • Insulin-like growth factor-I (IGF-I) has been implicated as a regulator of lens development. Experiments performed in the chick have indicated that IGF-I can stimulate lens fiber cell differentiation and may be involved in controlling lens polarization. To assess IGF-I activity on mammalian lens cells in vivo, we generated transgenic mice in which this factor was overexpressed from the alphaA-crystallin promoter. Interestingly, we observed no premature differentiation of lens epithelial cells. The pattern of lens polarization was perturbed, with an apparent expansion of the epithelial compartment towards the posterior lens pole. The distribution of immunoreactivity for MIP26 and p57(KIP2) and a modified pattern of proliferation suggested that this morphological change was best described as an expansion of the germinative and transitional zones. The expression of IGF-I signaling components in the normal transitional zone and expansion of the transitional zone in the transgenic lens both suggest that endogenous IGF-I may provide a spatial cue that helps to control the normal location of this domain.

subject areas

  • Animals
  • Cataract
  • Cell Differentiation
  • Cell Division
  • Immunohistochemistry
  • In Situ Hybridization
  • Insulin-Like Growth Factor I
  • Lens, Crystalline
  • Mice
  • Mice, Transgenic
  • Microscopy, Fluorescence
  • Models, Genetic
  • Phenotype
  • Promoter Regions, Genetic
  • Protein Structure, Tertiary
  • RNA, Messenger
  • Signal Transduction
  • Transgenes
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Research

keywords

  • alphaA-crystallin
  • insulin-like growth factor 1
  • lens development
  • lens polarization
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Identity

International Standard Serial Number (ISSN)

  • 0925-4773

Digital Object Identifier (DOI)

  • 10.1016/s0925-4773(00)00584-0

PubMed ID

  • 11231069
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Additional Document Info

start page

  • 167

end page

  • 174

volume

  • 101

issue

  • 1-2

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