Hematopoiesis in the bone marrow (BM) is maintained by specific interactions between both hematopoietic and non-hematopoietic stromal cells, which are mesenchymal stem cells (MSCs) capable of giving rise to several cell types. The human periodontal ligament (PDL), a tissue of ectomesenchymal origin, has been shown to also be a source of MSCs. We have investigated whether MSCs expanded from the PDL of healthy volunteers express characteristics similar to BM-derived stem cells using structural, immunocytochemical and molecular approaches. Their ability to support the growth of hematopoietic progenitors was also analyzed. The PDL-MSCs exhibited a fibroblast-like morphology and their chromatin was dispersed, indicating active gene transcription. The mesenchymal-related antigens CD90, CD29, CD166, CD105, and CD44 were homogeneously detected by cytofluorimetric analysis, whereas membrane CXCR4 was expressed only by a minority of cells. The PDL-MSCs differentiated in vitro into osteogenic and adipogenic cells. Immunolocalization of IL-7, IL-7Ralpha, SDF-1alpha, and CXCR4 resulted in a diffuse but specific labeling. RT-PCR analysis confirmed the expression of the above-mentioned transcripts. The cells spontaneously produced high levels of IL-7 and SDF-1alpha and were able to support the development and long-term maintenance of BM precursor cells more efficiently than murine stromal cells and similarly to normal BM human stromal cells. We examined IL-7 and SDF-1alpha secretion pathway during adipogenic and osteogenic differentiation. IL-7 increased during osteogenic and adipogenic differentiation, while the SDF-1alpha secretion was downregulated during osteogenic differentiation but increased during adipogenic induction. Our study provides evidence that in human PDL there is an accessible niche of MSCs showing the features of BM-derived MSCs.

Functional interleukin-7/interleukin-7Ralpha, and SDF-1alpha/CXCR4 are expressed by human periodontal ligament derived mesenchymal stem cells.

TRUBIANI, Oriana;ANTONUCCI, IVANA;DI PRIMIO, Roberto;CAPUTI, Sergio;PAGANELLI, Roberto
2008-01-01

Abstract

Hematopoiesis in the bone marrow (BM) is maintained by specific interactions between both hematopoietic and non-hematopoietic stromal cells, which are mesenchymal stem cells (MSCs) capable of giving rise to several cell types. The human periodontal ligament (PDL), a tissue of ectomesenchymal origin, has been shown to also be a source of MSCs. We have investigated whether MSCs expanded from the PDL of healthy volunteers express characteristics similar to BM-derived stem cells using structural, immunocytochemical and molecular approaches. Their ability to support the growth of hematopoietic progenitors was also analyzed. The PDL-MSCs exhibited a fibroblast-like morphology and their chromatin was dispersed, indicating active gene transcription. The mesenchymal-related antigens CD90, CD29, CD166, CD105, and CD44 were homogeneously detected by cytofluorimetric analysis, whereas membrane CXCR4 was expressed only by a minority of cells. The PDL-MSCs differentiated in vitro into osteogenic and adipogenic cells. Immunolocalization of IL-7, IL-7Ralpha, SDF-1alpha, and CXCR4 resulted in a diffuse but specific labeling. RT-PCR analysis confirmed the expression of the above-mentioned transcripts. The cells spontaneously produced high levels of IL-7 and SDF-1alpha and were able to support the development and long-term maintenance of BM precursor cells more efficiently than murine stromal cells and similarly to normal BM human stromal cells. We examined IL-7 and SDF-1alpha secretion pathway during adipogenic and osteogenic differentiation. IL-7 increased during osteogenic and adipogenic differentiation, while the SDF-1alpha secretion was downregulated during osteogenic differentiation but increased during adipogenic induction. Our study provides evidence that in human PDL there is an accessible niche of MSCs showing the features of BM-derived MSCs.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11564/109555
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