ArticleAmerican journal of physiology. Renal physiology2010
Telomerase immortalization of principal cells from mouse collecting duct.
Article in American journal of physiology. Renal physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Combination siRNA delivery as a therapeutic strategy for ADPKD.bioRxiv : the preprint server for biology · 2026Article
- Disruption of the human cystin-1 myristoyl-electrostatic switch causes polycystic kidney disease that phenocopies autosomal recessive polycystic kidney disease.Kidney international · 2026Article
- Senescence of bone marrow mesenchymal stromal cells: a narrative review of mechanisms, functional consequences, and rejuvenation strategies for age-related disorders.Stem cell research & therapy · 2025Review
- An Efficient Method for Immortalizing Mouse Embryonic Fibroblasts by CRISPR-mediated Deletion of theBio-protocol · 2025Article
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- An efficient method for immortalizing mouse embryonic fibroblasts.bioRxiv : the preprint server for biology · 2024Article
- Cystin is required for maintaining fibrocystin (FPC) levels and safeguarding proteome integrity in mouse renal epithelial cells: A mechanistic connection between the kidney defects in cpk mice and human ARPKD.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Chromosomal instability and its effect on cell lines.Cancer reports (Hoboken, N.J.) · 2023Review
- Differential regulation of MYC expression byFrontiers in cell and developmental biology · 2023Article
- Cystin genetic variants cause autosomal recessive polycystic kidney disease associated with altered Myc expression.Scientific reports · 2021Article
- The cpk model of recessive PKD shows glutamine dependence associated with the production of the oncometabolite 2-hydroxyglutarate.American journal of physiology. Renal physiology · 2015Article
- Inactivation of integrin-β1 prevents the development of polycystic kidney disease after the loss of polycystin-1.Journal of the American Society of Nephrology : JASN · 2015Article
- Culturing primary rat inner medullary collecting duct cells.Journal of visualized experiments : JoVE · 2013Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Recently, the use of overexpression of telomerase reverse transcriptase (TERT) has led to the generation of immortalized human cell lines. However, this cell immortalization approach has not been reported in well-differentiated mouse cells, such as renal epithelial cells. We sought to establish and then characterize a mouse collecting duct cell line, using ectopic expression of mTERT. Isolated primary cortical collecting duct (CCD) cell lines were transduced with mouse (m)TERT, using a lentiviral vector. mTERT-negative cells did not survive blasticidin selection, whereas mTERT-immortalized cells proliferated in selection media for over 40 subpassages. mTERT messenger RNA and telomerase activity was elevated in these cells, compared with an SV40-immortalized cell line. Flow cytometry with Dolichos biflorus agglutinin was used to select the CCD principal cells, and we designated this cell line mTERT-CCD. Cells were well differentiated and exhibited morphological characteristics typically found in renal epithelial cells, such as tight junction formation, microvilli, and primary cilia. Further characterization using standard immunofluorescence revealed abundant expression of aquaporin-2 and the vasopressin type 2 receptor. mTERT-CCD cells exhibited cAMP-stimulated/benzamil-inhibited whole cell currents. Whole cell patch-clamp currents were also enhanced after a 6-day treatment with aldosterone. In conclusion, we have successfully used mTERT to immortalize mouse collecting duct cells that retain the basic in vivo phenotypic characteristics of collecting duct cells. This technique should be valuable in generating cell lines from genetically engineered mouse models.
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