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Defective proliferative potential of MSCs from pediatric myelodysplastic syndrome patients is associated with cell senescence.

Authors: Qinghua Q. Liu, Hongbo H. Zhu, Jing J. Dong, Helou H. Li, Hong H. Zhang
Published: 10/01/2015, International journal of clinical and experimental pathology


Aberrant MSC function was shown to contribute to the pathophysiology of myelodysplastic syndromSe (MDS). In comparison to adult MDS, pediatric MDS displayed different features both in biologically and clinically. The mechanisms for adult MDS may not be applicable in pediatric MDS. However, understanding of the MSCs in pediatric MDS is lacking. In this study, we investigated the proliferation capacity of MSCs from pediatric MDS patients at clone cell level.

Material And Methods

Clone bone marrow MSCs were isolated from pediatric MDS patients and identified according to the criteria of the International Society for Cellular Therapy for MSCs. The proliferation capacity of pediatric MDS-derived MSCs was compared to healthy controls. Cell cycle was detected by flow cytometry following PI staining, as well as cell senescence was evaluated by β-galactosidase staining and telomere length.


Pediatric MDS-derived MSCs displayed similar basic biology characters as MSCs from healthy controls, including differentiation potential and surface markers. However, defective proliferative was displayed by pediatric MDS-derived MSCs. Pediatric MDS-derived MSCs were more prone to cellular senescence than healthy controls, and showed a decrease in the S phase.


Pediatric MDS-derived MSCs possess the basic characteristics of normal MSCs, but display defective proliferation, which may be associated with cell senescence.