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Lens transcriptome profile during cataract development in Mip-null mice.

Thomas M Bennett1, Yuefang Zhou1, Alan Shiels1

  • 1Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, MO, USA.

Biochemical and Biophysical Research Communications
|August 16, 2016
PubMed
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Loss of major intrinsic protein (MIP/AQP0) in the eye lens causes cataracts. Calpain hyper-activation, not red-ox changes, drives lens fiber cell death and cataract formation in MIP-null mice.

Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Genetics

Background:

  • Major intrinsic protein or aquaporin-0 (MIP/AQP0) is crucial for vertebrate eye lens function, acting as a water channel and cell-junction molecule.
  • Loss of MIP function leads to cataracts, but the underlying pathogenic mechanisms remain unclear.

Purpose of the Study:

  • To investigate lens transcriptome changes during cataract formation in mice lacking functional MIP (Mip-/-).
  • To identify key molecular events contributing to lens fiber cell degeneration and cataract development in the absence of MIP.

Main Methods:

  • Microarray-hybridization analysis was employed to profile gene expression in newborn (P1) and P7 Mip-/- mouse lenses.
  • TUNEL staining was used to assess DNA fragmentation, indicating cell death.
Keywords:
Aquaporin-0CalpainCataractHspb1LensTranscriptome

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  • Calpain activity was evaluated by measuring αII-spectrin proteolysis.
  • Red-ox status was assessed by measuring glutathione and free-radical levels.

    • Main Results:

    • A small percentage of genes (∼1.5%) showed differential regulation (>2-fold) in Mip-/- lenses.
    • Upregulated genes included those for mitochondrial translocase (Timmdc1), matrix metallopeptidase (Mmp2), Rho GTPase-interacting protein (Ubxn11), and transcription factor (Twist2).
    • Downregulated genes included proteasome subunit (Psmd8), ribonuclease (Pop4), and heat-shock protein (Hspb1).
    • Lens fiber cell degeneration correlated with increased TUNEL-positive nuclei and elevated calpain-mediated αII-spectrin breakdown.
    • Red-ox status remained similar to wild-type lenses.

    Conclusions:

    • Cataract formation in Mip-/- mice involves limited global transcriptome alterations.
    • Calpain hyper-activation is identified as a critical terminal event in lens fiber cell death during cataractogenesis.
    • MIP deficiency initiates a cascade leading to calpain-mediated proteolysis and subsequent lens opacity.