ArticleTransgenic research2012
Selective depletion of mouse kidney proximal straight tubule cells causes acute kidney injury.
Article in Transgenic research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- Multi-omic and spatial analysis of mouse kidneys highlights sex-specific differences in gene regulation across the lifespan.Nature genetics · 2025Article
- Article
- Albumin uptake and processing by the proximal tubule: physiological, pathological, and therapeutic implications.Physiological reviews · 2022Review
- Scattered Tubular Cells Markers in Macula Densa of Normal Human Adult Kidney.International journal of molecular sciences · 2022Article
- βAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2021Review
- Kidney Cells Regeneration: Dedifferentiation of Tubular Epithelium, Resident Stem Cells and Possible Niches for Renal Progenitors.International journal of molecular sciences · 2019Review
- Proximal TubuleThe Journal of pharmacology and experimental therapeutics · 2019Article
- Tubulointerstitial fibrosis can sensitize the kidney to subsequent glomerular injury.Kidney international · 2017Article
- PGC-1α attenuates hydrogen peroxide-induced apoptotic cell death by upregulating Nrf-2 via GSK3β inactivation mediated by activated p38 in HK-2 Cells.Scientific reports · 2017Article
- The proximal tubule is the primary target of injury and progression of kidney disease: role of the glomerulotubular junction.American journal of physiology. Renal physiology · 2016Review
- Simultaneous deletion of Bax and Bak is required to prevent apoptosis and interstitial fibrosis in obstructive nephropathy.American journal of physiology. Renal physiology · 2015Article
- MG53-mediated cell membrane repair protects against acute kidney injury.Science translational medicine · 2015Article
- Natural killer T (NKT) cells accelerate Shiga toxin type 2 (Stx2) pathology in mice.Frontiers in microbiology · 2015Article
- Letter to the editor: "Quantifying albumin permeability with multiphoton microscopy: why the difference?".American journal of physiology. Renal physiology · 2014Article
- The proximal tubule and albuminuria: really!Journal of the American Society of Nephrology : JASN · 2014Review
- Using 2-photon microscopy to understand albuminuria.Transactions of the American Clinical and Climatological Association · 2014Review
- Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proximal straight tubule (S3 segment) of the kidney is highly susceptible to ischemia and toxic insults but has a remarkable capacity to repair its structure and function. In response to such injuries, complex processes take place to regenerate the epithelial cells of the S3 segment; however, the precise molecular mechanisms of this regeneration are still being investigated. By applying the "toxin receptor mediated cell knockout" method under the control of the S3 segment-specific promoter/enhancer, Gsl5, which drives core 2 β-1,6-N-acetylglucosaminyltransferase gene expression, we established a transgenic mouse line expressing the human diphtheria toxin (DT) receptor only in the S3 segment. The administration of DT to these transgenic mice caused the selective ablation of S3 segment cells in a dose-dependent manner, and transgenic mice exhibited polyuria containing serum albumin and subsequently developed oliguria. An increase in the concentration of blood urea nitrogen was also observed, and the peak BUN levels occurred 3-7 days after DT administration. Histological analysis revealed that the most severe injury occurred in the S3 segments of the proximal tubule, in which tubular cells were exfoliated into the tubular lumen. In addition, aquaporin 7, which is localized exclusively to the S3 segment, was diminished. These results indicate that this transgenic mouse can suffer acute kidney injury (AKI) caused by S3 segment-specific damage after DT administration. This transgenic line offers an excellent model to uncover the mechanisms of AKI and its rapid recovery.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.