- Meeting abstract
- Open Access
HTLV-1 affects the adipogenic differentiation of human mesenchymal stem cells
© Rodrigues et al; licensee BioMed Central Ltd. 2011
- Published: 6 June 2011
- Bone Marrow
- Mesenchymal Stem Cell
- Bone Marrow Cell
- Differentiation Potential
- Adipogenic Differentiation
Mesenchymal stem cells (MSCs) are multipotent cells mainly found in the bone marrow (BM) and are considered to support human hematopoiesis. During HTLV-1 infection, T cells that are infected may migrate to the BM, and establish a progressive viral invasion. The persistence of these cells in the BM may affect the function of the resident BM cells and the biological properties of this microenvironment. However, the exact mechanisms of this phenomenon and the relative contribution of HTLV-1 to BM cell dysfunction remain to be elucidated. In this study, we evaluated the ability of HTLV-1 to disturb MSCs normal functions.
Human MSCs were cultured on the presence of MT-2 cell line. MSCs markers and adipogenic differentiation potential was evaluated.
We observed that MSCs that had contact with HTLV-1 were able to differentiate into adipocytes. However, gene expression of PPARG, cell morphology and intracellular lipid formation analyses revealed that adipogenic differentiation of MSCs that were exposed to HTLV-1 was decreased compared to MSCs not exposed (p<0.03). In addition, analyses by flow cytometry showed a reduction of the expression of MSCs markers (CD271 and HLA-DR) in MSCs that had contact with HTLV-1.
HTLV-1 caused significant changes in the characteristics and functions of MSCs. This finding suggests the importance of HTLV infection on MSCs, and this could contribute to the understanding the viral infection mechanisms and pathogenesis.
Financial support: CTC, INCTC, FAPESP, FUNDHERP and CNPq.
This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.