Prominin-1 (CD133): New Insights on Stem & Cancer Stem Cell Biology by Denis Corbeil

Author:Denis Corbeil
Language: eng
Format: epub
Publisher: Springer New York, New York, NY

8.4.2 Involvement of CD133+ Cells in Renal Fibrosis

A recent study by Simone and colleagues showed the possible maldifferentiation of CD133+ renal progenitors in myofibroblasts after delayed graft function (DGF) (41). DGF, defined as the requirement for dialysis in the first week after transplantation, is a common complication after renal transplantation; it is caused by acute kidney injury, and it is characterized by tissue inflammation and involvement of many cellular and soluble mediators. In particular, after DGF, the occurrence of oxidative stimuli such as oxygen radicals and presence of the bone morphogenetic protein-2 (BMP-2) in the tissue microenvironment promote the expression of α-smooth muscle cell actin in CD133+ cells. The acquisition of a myofibroblast marker by CD133+ cells clearly indicates their commitment toward a myofibroblastic phenotype that may be relevant in tissue fibrosis. This process of maldifferentiation could be important for progression of renal damage. An antifibrotic effect of the antioxidant N-acetyl-cysteine can be envisaged in this pathological setting.

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