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Isolation, Characterization, And High Throughput Extracellular Flux Analysis of Mouse Primary Renal Tubular Epithelial Cells
Published on: June 20, 2018
Role of tubular cells in progressive renal disease
C van Kooten1, A M Langers, J A Bruijn
1Department of Nephrology, Leiden University Medical Center, Leiden, the Netherlands. Kooten@Rullf2.Medfac.LeidenUniv.nl
Abstract:
It is generally accepted that the progressive loss of kidney function results from a pathogenic process that is independent of the original etiology, functioning as a final common pathway. Part of this response is characterized by triggering of interstitial infiltration and induction of tubular damage. As a consequence, tubular epithelial cells (TEC) can become activated and begin to express several inflammatory mediators. In the present review, we will summarize the potential role of TEC in progressive renal disease. Much emphasis will be put on studies using in vitro cultured TEC. These studies have provided more insight into the different signals involved in the regulation of the production of inflammatory mediators like complement, cytokines and chemokines, as well as progression factors like growth factors and matrix component by TEC.
Insights
Tubular epithelial cells (TEC) play a key role in kidney disease progression, independent of the initial cause. Understanding TEC activation and inflammatory mediator production is crucial for developing new therapeutic strategies.
Area of Science:
- Nephrology
- Renal Pathophysiology
- Cell Biology
Background:
- Progressive kidney function loss often follows a common pathway, involving interstitial infiltration and tubular damage.
- Tubular epithelial cells (TEC) become activated during this process, producing inflammatory mediators.
- The specific role of TEC in the common pathway of progressive renal disease requires further elucidation.
Purpose of the Study:
- To review the potential role of TEC in progressive renal disease.
- To highlight insights gained from in vitro studies of cultured TEC.
- To summarize regulatory signals for inflammatory and progression factor production by TEC.
Main Methods:
- Review of existing literature focusing on TEC in progressive renal disease.
- Emphasis on studies utilizing in vitro cultured TEC models.
- Analysis of signaling pathways regulating mediator production in TEC.
Main Results:
- Activated TEC contribute to renal inflammation by producing complement, cytokines, and chemokines.
- TEC also produce growth factors and matrix components, influencing disease progression.
- In vitro studies have identified key signals regulating these TEC-derived factors.
Conclusions:
- TEC are central players in the common pathway of progressive renal disease.
- Understanding TEC-mediated inflammation and matrix production is vital for therapeutic development.
- Targeting TEC activation and mediator release may offer novel treatment strategies for kidney disease.
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