ArticleBiochimica et biophysica acta2016
Lens ER-stress response during cataract development in Mip-mutant mice.
Article in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed.
- CatExperimental eye research · 2026Article
- Loss of alpha-kinase 1 contributes to the formation of congenital cataracts in mice.Cellular & molecular biology letters · 2025Article
- Whole Exome Sequencing Study Uncovers Novel Candidate Genes and Protein-Coding Variants for Cataract.Investigative ophthalmology & visual science · 2025Article
- Functional characterization of CatExperimental eye research · 2025Article
- Role of C/EBP Homologous Protein (CHOP) and Nupr1 Interaction in Endoplasmic Reticulum Stress-Induced Apoptosis of Lens Epithelial Cells.Molecular biotechnology · 2025Article
- Through theGenes · 2024Review
- Glutamate is effective in decreasing opacity formed in galactose-induced cataract model.Scientific reports · 2024Article
- A Cataract-Causing Mutation in the TRPM3 Cation Channel Disrupts Calcium Dynamics in the Lens.Cells · 2024Article
- CHAC1: a master regulator of oxidative stress and ferroptosis in human diseases and cancers.Frontiers in cell and developmental biology · 2024Review
- Unbalanced redox status network as an early pathological event in congenital cataracts.Redox biology · 2023Article
- Charged multivesicular body protein 4b forms complexes with gap junction proteins during lens fiber cell differentiation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Article
- Deficiency of Jamc Leads to Congenital Nuclear Cataract and Activates the Unfolded Protein Response in Mouse Lenses.Investigative ophthalmology & visual science · 2022Article
- Changes in DNA methylation hallmark alterations in chromatin accessibility and gene expression for eye lens differentiation.Epigenetics & chromatin · 2022Article
- High glucose induces HSP47 expression and promotes the secretion of inflammatory factors through the IRE1α/XBP1/HIF-1α pathway in retinal Müller cells.Experimental and therapeutic medicine · 2021Article
- Article
- Inherited cataracts: Genetic mechanisms and pathways new and old.Experimental eye research · 2021Review
- 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
- Endoplasmic reticulum stress: New insights into the pathogenesis and treatment of retinal degenerative diseases.Progress in retinal and eye research · 2020Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Major intrinsic protein (MIP) is a functional water-channel (AQP0) that also plays a key role in establishing lens fiber cell architecture. Genetic variants of MIP have been associated with inherited and age-related forms of cataract; however, the underlying pathogenic mechanisms are unclear. Here we have used lens transcriptome profiling by microarray-hybridization and qPCR to identify pathogenic changes during cataract development in Mip-mutant (Lop/+) mice. In postnatal Lop/+ lenses (P7) 99 genes were up-regulated and 75 were down-regulated (>2-fold, p=<0.05) when compared with wild-type. A pathway analysis of up-regulated genes in the Lop/+ lens (P7) was consistent with endoplasmic reticulum (ER)-stress and activation of the unfolded protein response (UPR). The most up-regulated UPR genes (>4-fold) in the Lop/+ lens included Chac1>Ddit3>Atf3>Trib3>Xbp1 and the most down-regulated genes (>5-fold) included two anti-oxidant genes, Hspb1 and Hmox1. Lop/+ lenses were further characterized by abundant TUNEL-positive nuclei within central degenerating fiber cells, glutathione depletion, free-radical overproduction, and calpain hyper-activation. These data suggest that Lop/+ lenses undergo proteotoxic ER-stress induced cell-death resulting from prolonged activation of the Eif2ak3/Perk-Atf4-Ddit3-Chac1 branch of the UPR coupled with severe oxidative-stress.
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