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Regeneration of Glomerular Podocytes by Human Renal Progenitors

Elisa Ronconi^*, Costanza Sagrinati^*, Maria Lucia Angelotti^*, Elena Lazzeri^*, Benedetta Mazzinghi^*, Lara Ballerini^*, Eliana Parente^*, Francesca Becherucci^*, Mauro Gacci, Marco Carini, Enrico Maggi^*, Mario Serio^*, Gabriella Barbara Vannelli, Laura Lasagni^*, Sergio Romagnani^* and Paola Romagnani^*

^* Excellence Center for Research, Transfer and High Education Denothe, Department of Medical and Surgical Critical Care, and Department of Anatomy, University of Florence, Florence, Italy

Correspondence: Dr. Paola Romagnani, Department of Clinical Pathophysiology, Nephrology Section, University of Florence, Viale Pieraccini 6, 50139, Firenze, Italy. Phone: ++39554271356; Fax: ++39554271357; E-mail: p.romagnani{at}dfc.unifi.it

Received for publication July 11, 2008. Accepted for publication September 21, 2008.

Depletion of podocytes, common to glomerular diseases in general, plays a role in the pathogenesis of glomerulosclerosis. Whether podocyte injury in adulthood can be repaired has not been established. Here, we demonstrate that in the adult human kidney, CD133+CD24+ cells consist of a hierarchical population of progenitors that are arranged in a precise sequence within Bowman's capsule and exhibit heterogeneous potential for differentiation and regeneration. Cells localized to the urinary pole that expressed CD133 and CD24, but not podocyte markers (CD133+CD24+PDX– cells), could regenerate both tubular cells and podocytes. In contrast, cells localized between the urinary pole and vascular pole that expressed both progenitor and podocytes markers (CD133+CD24+PDX+) could regenerate only podocytes. Finally, cells localized to the vascular pole did not exhibit progenitor markers, but displayed phenotypic features of differentiated podocytes (CD133–CD24–PDX+ cells). Injection of CD133+CD24+PDX– cells, but not CD133+CD24+PDX+ or CD133-CD24– cells, into mice with adriamycin-induced nephropathy reduced proteinuria and improved chronic glomerular damage, suggesting that CD133+CD24+PDX– cells could potentially treat glomerular disorders characterized by podocyte injury, proteinuria, and progressive glomerulosclerosis.

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