1. ¹Department of Pediatrics and Laboratory of Regenerative Nephrology, Edmond and Lili Safra Children's Hospital, Sheba Medical Center, Tel Hashomer, Israel
2. ²Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel
3. ³Centro Andaluz de Biologia del Desarrollo (CABD), Consejo Superior de Investigaciones Cientificas, Universidad Pablo de Olavide, Seville, Spain
4. ⁴Department of Pediatric Hemato-Oncology and the Cancer Research Center, Safra Children's Hospital, Sheba Medical Center, Tel Hashomer, Israel

Correspondence: Dr B Dekel, Department of Pediatrics and Laboratory of Regenerative Nephrology, Sheba Medical Center, Tel Hashomer, 52621, Israel. E-mail: benjamin.dekel@sheba.health.gov.il

⁵These authors equally contributed to this paper.

Received 30 April 2007; Revised 17 July 2007; Accepted 30 July 2007; Published online 27 September 2007.

Abstract

Early in mammalian development, the stem cell leukemia (SCL/TAL1) gene and its distinct 3' enhancer (SCL 3'En) specify bipotential progenitor cells that give rise to blood and endothelium, thus termed hemangioblasts. We have previously detected a minor population of SCL (+) cells in the postnatal kidney. Here, we demonstrate that cells expressing the SCL 3'En in the adult kidney are comprised of CD45+CD31- hematopoietic cells, CD45-CD31+ endothelial cells and CD45-CD31- interstitial cells. Creation of bone marrow chimeras of SCL 3'En transgenic mice into wild-type hosts shows that all three types of SCL 3'En-expressing cells in the adult kidney can originate from the bone marrow. Ischemia/reperfusion injury to the adult kidney of SCL 3'En transgenic mice results in the intrarenal elevation of SCL and FLK1 mRNA levels and of cells expressing hem-endothelial progenitor markers (CD45, CD34, c-Kit and FLK1). Furthermore, analysis of SCL 3'En in the ischemic kidneys reveals an increase in the abundance of SCL 3'En-expressing cells, predominantly within the CD45 (+) hematopoietic fraction and to a lesser extent in the CD45 (-) fraction. Our results suggest organ-injury-induced reactivation of bone marrow-derived hemangioblasts and possible local angioblastic progenitors expressing SCL and SCL 3'En.