ArticleInvestigative ophthalmology & visual science2017
Conditionally Immortal Slc4a11-/- Mouse Corneal Endothelial Cell Line Recapitulates Disrupted Glutaminolysis Seen in Slc4a11-/- Mouse Model.
Article in Investigative ophthalmology & visual science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- An Optimized Mechanical Peeling Protocol for Mouse Corneal Endothelium.Bioengineering (Basel, Switzerland) · 2026Article
- Sex differences in congenital hereditary endothelial dystrophy (CHED) and Slc4a11Biology of sex differences · 2026Article
- A Murine Model of HSV-1-Induced Corneal Endotheliitis: Primary Infection, Latency, and Recurrence.Investigative ophthalmology & visual science · 2026Article
- SLC4A11 is a targetable marker correlated with therapeutic responses in ovarian cancer.Journal of ovarian research · 2025Article
- Review
- Investigation of the functional impact of CHED- and FECD4-associated SLC4A11 mutations in human corneal endothelial cells.PloS one · 2024Article
- Corneal Endothelial-like Cells Derived from Induced Pluripotent Stem Cells for Cell Therapy.International journal of molecular sciences · 2023Review
- Corneal Edema in InducibleCells · 2023Article
- A mesenchymal to epithelial switch in Fgf10 expression specifies an evolutionary-conserved population of ionocytes in salivary glands.Cell reports · 2022Article
- The HCells · 2022Review
- RNA sequencing uncovers alterations in corneal endothelial metabolism, pump and barrier functions of Slc4a11 KO mice.Experimental eye research · 2022Article
- Mitochondrial ROS inFrontiers in cell and developmental biology · 2022Article
- Altered gene expression in slc4a11Scientific reports · 2021Article
- Mitochondrial Targeting of the Ammonia-Sensitive Uncoupler SLC4A11 by the Chaperone-Mediated Carrier Pathway in Corneal Endothelium.Investigative ophthalmology & visual science · 2021Article
- Mitochondrial ROS Induced Lysosomal Dysfunction and Autophagy Impairment in an Animal Model of Congenital Hereditary Endothelial Dystrophy.Investigative ophthalmology & visual science · 2021Article
- Inducible Slc4a11 Knockout Triggers Corneal Edema Through Perturbation of Corneal Endothelial Pump.Investigative ophthalmology & visual science · 2021Article
- Fuchs endothelial corneal dystrophy: The vicious cycle of Fuchs pathogenesis.Progress in retinal and eye research · 2021Review
- Bicarbonate activates glycolysis and lactate production in corneal endothelial cells by increased pHExperimental eye research · 2020Article
- Energy Shortage in Human and Mouse Models of SLC4A11-Associated Corneal Endothelial Dystrophies.Investigative ophthalmology & visual science · 2020Article
- SLC4A11 function: evidence for HAmerican journal of physiology. Cell physiology · 2020Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Purpose: To establish conditionally immortal mouse corneal endothelial cell lines with genetically matched Slc4a11+/+ and Slc4a11-/- mice as a model for investigating pathology and therapies for SLC4A11 associated congenital hereditary endothelial dystrophy (CHED) and Fuchs' endothelial corneal dystrophy. Methods: We intercrossed H-2Kb-tsA58 mice (Immortomouse) expressing an IFN-γ dependent and temperature-sensitive mutant of the SV40 large T antigen (tsTAg) with Slc4a11+/+ and Slc4a11-/- C57BL/6 mice. The growth characteristics of the cell lines was assessed by doubling time. Ion transport activities (Na+/H+ exchange, bicarbonate, lactate, and Slc4a11 ammonia transport) were analyzed by intracellular pH measurement. The metabolic status of the cell lines was assessed by analyzing TCA cycle intermediates via gas chromatography mass spectrometry (GC-MS). Results: The immortalized Slc4a11+/+ and Slc4a11-/- mouse corneal endothelial cells (MCECs) remained proliferative through passage 49 and maintained similar active ion transport activity. As expected, proliferation was temperature sensitive and IFN-γ dependent. Slc4a11-/- MCECs exhibited decreased proliferative capacity, reduced NH3:H+ transport, altered expression of glutaminolysis enzymes similar to the Slc4a11-/- mouse, and reduced proportion of TCA cycle intermediates derived from glutamine with compensatory increases in glucose flux compared with Slc4a11+/+ MCECs. Conclusions: This is the first report of the immortalization of MCECs. Ion transport of the immortalized endothelial cells remains active, except for NH3:H+ transporter activity in Slc4a11-/- MCECs. Furthermore, Slc4a11-/- MCECs recapitulate the glutaminolysis defects observed in Slc4a11-/- mouse corneal endothelium, providing an excellent tool to study the pathogenesis of SLC4A11 mutations associated with corneal endothelial dystrophies and to screen potential therapeutic agents.
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