ArticleBiochemical and biophysical research communications2016
Lens transcriptome profile during cataract development in Mip-null mice.
Article in Biochemical and biophysical research communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Differentiation of mesenchymal stem cells towards lens epithelial stem cells based on three-dimensional bio-printed matrix.Frontiers in cell and developmental biology · 2024Article
- Application of transgenic mice to the molecular pathogenesis of cataract.International journal of ophthalmology · 2024Review
- Integrative transcriptomic profiling of ncRNAs and mRNAs in developing mouse lens.Frontiers in genetics · 2024Article
- RNA-Seq analysis in giant pandas reveals the differential expression of multiple genes involved in cataract formation.BMC genomic data · 2021Article
- Mutation of the TRPM3 cation channel underlies progressive cataract development and lens calcification associated with pro-fibrotic and immune cell responses.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- The relationship between major intrinsic protein genes and cataract.International ophthalmology · 2021Review
- Proteome-transcriptome analysis and proteome remodeling in mouse lens epithelium and fibers.Experimental eye research · 2019Article
- Acute lens opacity induced by different kinds of anesthetic drugs in mice.International journal of ophthalmology · 2019Article
- Spatial Analysis of Single Fiber Cells of the Developing Ocular Lens Reveals Regulated Heterogeneity of Gene Expression.iScience · 2018Article
- Aquaporin 0 Modulates Lens Gap Junctions in the Presence of Lens-Specific Beaded Filament Proteins.Investigative ophthalmology & visual science · 2017Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Major intrinsic protein or aquaporin-0 (MIP/AQP0) functions as a water channel and a cell-junction molecule in the vertebrate eye lens. Loss of MIP function in the lens leads to degraded optical quality and cataract formation by pathogenic mechanisms that are unclear. Here we have used microarray-hybridization analysis to detect lens transcriptome changes during cataract formation in mice that are functionally null for MIP (Mip-/-). In newborn Mip-/- lenses (P1) 11 genes were up-regulated and 18 were down-regulated (>2-fold, p=<0.05) and a similar number of genes was differentially regulated at P7. The most up-regulated genes (>6-fold) in the Mip-/- lens at P1 included those coding for a mitochondrial translocase (Timmdc1), a matrix metallopeptidase (Mmp2), a Rho GTPase-interacting protein (Ubxn11) and a transcription factor (Twist2). Apart from Mip, the most down-regulated genes (>4-fold) in the Mip-/- lens at P1 included those coding for a proteasome sub-unit (Psmd8), a ribonuclease (Pop4), and a heat-shock protein (Hspb1). Lens fiber cell degeneration in the Mip-/- lens was associated with increased numbers of TUNEL-positive cell nuclei and dramatically elevated levels of calpain-mediated proteolysis of αII-spectrin. However red-ox status, measured by glutathione and free-radical levels, was similar to that of wild-type. These data suggest that while relatively few genes (∼1.5% of the transcriptome) were differentially regulated >2-fold in the Mip-/- lens, calpain hyper-activation acts as a terminal pathogenic event during lens fiber cell death and cataract formation.
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