Abstract Title:

Fancd2-/- mice have hematopoietic defects that can be partially corrected by resveratrol.

Abstract Source:

Blood. 2010 Dec 9;116(24):5140-8. Epub 2010 Sep 8. PMID: 20826722

Abstract Author(s):

Qing-Shuo Zhang, Laura Marquez-Loza, Laura Eaton, Andrew W Duncan, Devorah C Goldman, Praveen Anur, Kevin Watanabe-Smith, R Keaney Rathbun, William H Fleming, Grover C Bagby, Markus Grompe

Article Affiliation:

Oregon Stem Cell Center, Department of Pediatrics, Oregon Health&Science University, Portland, OR, USA. zhangqi@ohsu.edu


Progressive bone marrow failure is a major cause of morbidity and mortality in human Fanconi Anemia patients. In an effort to develop a Fanconi Anemia murine model to study bone marrow failure, we found that Fancd2(-/-) mice have readily measurable hematopoietic defects. Fancd2 deficiency was associated with a significant decline in the size of the c-Kit(+)Sca-1(+)Lineage(-) (KSL) pool and reduced stem cell repopulation and spleen colony-forming capacity. Fancd2(-/-) KSL cells showed an abnormal cell cycle status and loss of quiescence. In addition, the supportive function of the marrow microenvironment was compromised in Fancd2(-/-) mice. Treatment with Sirt1-mimetic and the antioxidant drug, resveratrol, maintained Fancd2(-/-) KSL cells in quiescence, improved the marrow microenvironment, partially corrected the abnormal cell cycle status, and significantly improved the spleen colony-forming capacity of Fancd2(-/-) bone marrow cells. We conclude that Fancd2(-/-) mice have readily quantifiable hematopoietic defects, and that this model is well suited for pharmacologic screening studies.

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