Biologic characteristics of bone marrow-derived mesenchymal stem cells from a patient with thalassemia syndrome

Summary Introduction:  Mesenchymal stem cells (MSCs) are capable of self‐renewal and differentiating morphologically and functionally into several mesenchymal tissues. There have been contrasting data on whether MSCs are altered in various hematologic disorders. Methods:  We isolated bone marrow (BM...

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Veröffentlicht in:International journal of laboratory hematology 2011-06, Vol.33 (3), p.281-289
Hauptverfasser: YOON, J. S., KIM, E. S., HWANG, D. W., CHOI, J. Y., KIM, B. K., PARK, B. B., CHOI, J. H., LEE, Y. Y.
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Sprache:eng
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Zusammenfassung:Summary Introduction:  Mesenchymal stem cells (MSCs) are capable of self‐renewal and differentiating morphologically and functionally into several mesenchymal tissues. There have been contrasting data on whether MSCs are altered in various hematologic disorders. Methods:  We isolated bone marrow (BM)–derived MSCs from a patient with thalassemia syndrome to compare phenotypic and functional characteristics to those from normal healthy donor. Results:  No differences were observed between MSCs from thalassemia syndrome (T‐MSCs) and those from normal healthy donor in terms of morphology, phenotype, karyotype, multidifferentiation capacity. In mixed lymphocyte reaction, T‐MSCs strongly inhibited the proliferation of allogeneic T cells in association with reduced proportion of CD3+, CD4+, and CD8+ cells. Furthermore, the fraction of Treg cells was increased under the culture with T‐MSCs, suggesting that T‐MSCs exert normal immunomodulatory function. In addition, T‐MSCs expressed hematopoietic cytokines and supported hematopoiesis, which was comparable to those from normal BM‐derived MSCs. Conclusion:  T‐MSCs exhibited normal phenotype, karyotype as well as normal immunomodulatory function, and autologous MSCs from patients with thalassemia syndrome may be an attractive source of stem cell in terms of hematopoietic support as well as immunomodulatory activity.
ISSN:1751-5521
1751-553X
DOI:10.1111/j.1751-553X.2010.01285.x