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Human Bone Marrow Mesenchymal Stem Cells

Human bone marrow mesenchymal stem cells expressing SDF-1 promote hematopoietic stem cell function of human mobilised peripheral blood CD34+ cells in vivo and in vitro

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Pages 230-237 | Received 21 Jun 2009, Accepted 25 Sep 2009, Published online: 04 Mar 2010
 

Abstract

Purpose: There is mounting evidence demonstrating that stromal cell derived factor-1 (SDF-1) plays an important role in homing of hematopoietic progenitor cells to bone marrow. This study was aimed to assess whether bone marrow mesenchymal stem cells overexpressing exogenous SDF-1 could synergistically promote the homing of CD34+ (Cluster of Differentiation [CD]) cells to bone marrow of lethally irradiated severe combined immunodeficiency (SCID) mice.

Methods: Human SDF-1 complementary Deoxyribonucleic acid (cDNA) was transfected into bone marrow-derived mesenchymal stem cells with recombinant lentiviral vector. The expression of SDF-1 was detected by real-time Polymerase Chain Reaction (PCR) and Enzyme-Linked Immunosorbent Assay (ELISA), and the ex vivo chemotaxis function on CD34+ cells was measured by coculture system and Transwell system. SDF-1 gene-modified mesenchymal stem cell (MSC) and CD34+ cells were infused into lethally irradiated SCID mice and the hematopoietic reconstitution in the recipient mice was examined.

Results: Messenger ribonucleic acid (mRNA) and protein of SDF-1 in infected MSC were significantly higher than that of the non-infected control MSC (p < 0.05). The infected MSC have significant chemotaxis effect on CD34+ cells in vitro and promote hematopoietic reconstitution after CD34+ cell transplantation in vivo.

Conclusion: MSC with high-level expression of SDF-1 can synergistically promote hematopoietic reconstitution after CD34+ cell transplantation in lethally irradiated SCID mice.

Acknowledgements

This work was supported by the Funds for State Key Laboratory of Trauma, Burns and Combined Injury (2003).

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

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