Tubular Cell Proliferation
Tubular Cell Proliferation - Related Videos
06:32
Development of Human Renal Tubular Epithelial Cell Primary Cultures in Monolayers and Three-Dimensional Conditions
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2025
Here, we describe the protocols for obtaining primary cultures of human renal tubular epithelial cells (HRTEC) from the kidney cortex to develop monolayers and three-dimensional cultures on an extracellular matrix (3D-HRTEC).
03:21
Murine Renal Cell Isolation: A Technique to Isolate and Generate Primary Culture of Renal Tubular Epithelial Cells
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2023
In this video, we demonstrate the steps to isolate and purify renal tubular epithelial cells for a wide range of molecular biology and cell culture studies.
06:23
Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells
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2025
Here, we describe an in vitro protocol to model hypoxia/reoxygenation damage in the highly metabolic proximal tubular epithelial cells. This model is designed to induce metabolic stress-induced damage, which can be measured through the expression of proximal tubule damage markers and assessment of mitochondrial respiratory function.
06:14
Assessment of Mitochondrial Fission/Fusion Dynamics in Kidney Proximal Tubular Cells
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2025
This article describes the use of confocal microscopy and ImageJ to assess mitochondrial fission/fusion dynamics via Dendra2 photo-switching fluorescence.
22:49
Optimized Staining and Proliferation Modeling Methods for Cell Division Monitoring using Cell Tracking Dyes
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Cited by 45 •
2012
Successful use of cell tracking dyes to monitor immune cell function and proliferation involves several critical steps. We describe methods for: 1) obtaining bright, uniform, reproducible label-ing with membrane dyes; 2) selecting fluorochromes and data acquisition conditions; and 3) choosing a model to quantify cell proliferation based on dye dilution.
FAQs
Surviving tubular epithelial cells serve as the repair-capable population after injury. Damage or physiological signals can prompt these cells to re-enter the cell cycle, replicate their DNA, and divide. This sequence expands the epithelial population without requiring a separate cell source, making it central to restoring the injured tubular lining.
Cell-cycle re-entry is important because proliferation alone is not the endpoint of repair. Newly divided epithelial cells must contribute to rebuilding the tubular lining so transport functions can return. In this context, the outcome of proliferation is judged by whether it supports epithelial restoration, rather than simply by an increased cell number.
Physiological signals and injury-related signals may both activate the response, but their context differs. A controlled response can support maintenance or recovery after acute kidney injury, whereas persistent disease raises concern that repair may become associated with maladaptive tissue remodeling. This distinction helps explain why proliferation is relevant to both recovery and chronic kidney disease.
Laboratory models of tubular cells let investigators examine the proliferative response in a controlled setting. They are used to study kidney injury, nephrotoxicity, and regenerative therapies. These models also provide a way to explore whether an intervention encourages repair while avoiding changes linked to maladaptive tissue remodeling, supporting the evaluation of potential treatments.
Because tubular cells form the epithelial lining responsible for tubular transport, their proliferative response can serve as a research focus when investigating nephrotoxicity. Laboratory studies can examine how damaging exposures affect the capacity of tubular cells to re-enter the cell cycle and restore the epithelium. This connects cellular behavior with kidney-injury research.
Regenerative strategies seek to promote repair after tubular injury, so proliferation is a potential cellular response to support. However, increasing cell division is not sufficient by itself: the desired outcome is restoration of the tubular epithelium and its transport functions without driving maladaptive tissue remodeling. This balance is central to evaluating candidate treatments.