1. ¹Laboratory of Cancer Gene Therapy, Division of Cellular and Molecular Research, National Cancer Centre, Singapore, Singapore
2. ²Division of BioEngineering, School of Chemical and Biomedical Engineering, Nanyang Technological University, Singapore, Singapore
3. ³Research and Development Unit, National Heart Centre, Singapore, Singapore
4. ⁴Department of Orthopedic, Singapore General Hospital, Singapore, Singapore

Correspondence: Dr PYP Lam, Laboratory of Cancer Gene Therapy, Division of Cellular and Molecular Research, National Cancer Centre, 11 Hospital Drive, Singapore 169610, Singapore. E-mail: cmrlyp@nccs.com.sg

Received 11 October 2007; Revised 11 January 2008; Accepted 24 February 2008; Published online 6 June 2008.

Abstract

Human bone marrow-derived mesenchymal stem cells (BM-hMSCs) are nonhematopoietic stem cells that have the potential to differentiate into adipocytes, osteocytes and chondrocytes. Because of its propensity to migrate to the sites of injury and the ability to expand them rapidly, BM-hMSCs have been exploited as potential gene transfer vehicles to deliver therapeutic genes. Herein, we evaluated the feasibility of employing herpes simplex virus type I (HSV-1) amplicon viral vector as a gene delivery vector to BM-hMSCs. High transduction efficiencies were consistently observed in different isolates of BM-hMSCs following infection with HSV-1 amplicon viral vectors. Furthermore, we demonstrated that transduction with HSV-1 amplicon viral vector did not alter the intrinsic properties of the BM-hMSCs. The morphology and cellular proliferation of the transduced BM-hMSCs were not altered. Chromosomal stability, as confirmed by karyotyping and soft agar colony assays, of the transduced BM-hMSCs was not affected. Similarly, transduction with HSV-1 amplicon viral vectors has no effect on the pluripotent differentiation potential and the tumor tropism of BM-hMSCs. Taken together, these results demonstrated that BM-hMSCs could be transduced efficiently by HSV-1 amplicon viral vector in an 'inert' manner and thus enable strategies to express potential therapeutic genes in BM-hMSCs.