AI Article Synopsis
- - Tissue fibrosis and reduced blood vessel density are major issues in kidney disease, with CD248 being a protein linked to these problems in cells of damaged kidneys.
- - In a study using a kidney injury model, researchers found that mice without the CD248 gene showed less fibrosis and reduced blood vessel loss after injury, possibly due to changes in how cells called pericytes behaved.
- - The findings suggest that targeting CD248 could help prevent kidney damage by altering the activity of harmful stroma cells, offering a potential therapeutic approach for kidney disease.
Article Abstract
Background: Tissue fibrosis and microvascular rarefaction are hallmarks of progressive renal disease. CD248 is a transmembrane glycoprotein expressed by key effector cells within the stroma of fibrotic kidneys including pericytes, myofibroblasts and stromal fibroblasts. In human disease, increased expression of CD248 by stromal cells predicts progression to end-stage renal failure. We therefore, hypothesized that the genetic deletion of the CD248 gene would protect against fibrosis following kidney injury.
Methods: Using the unilateral ureteral obstruction (UUO) model of renal fibrosis, we investigated the effect of genetic deletion of CD248 on post obstructive kidney fibrosis.
Results: CD248 null mice were protected from fibrosis and microvascular rarefaction following UUO. Although the precise mechanism is not known, this may to be due to a stabilizing effect of pericytes with less migration and differentiation of pericytes toward a myofibroblast phenotype in CD248-/- mice. CD248-/- fibroblasts also proliferated less and deposited less collagen in vitro.
Conclusion: These studies suggest that CD248 stromal cells have a pathogenic role in renal fibrosis and that targeting CD248 is effective at inhibiting both microvascular rarefaction and renal fibrosis through modulation of pericyte and stromal cell function.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4872467 | PMC |
| http://dx.doi.org/10.1159/000438754 | DOI Listing |
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