Abstract
Human bone marrow-derived mesenchymal stromal cells (MSCs) have been investigated in numerous disease settings involving impaired regeneration because of the crucial role they play in tissue maintenance and repair. Considering the number of comorbidities associated with type 2 diabetes mellitus (T2DM), the hypothesis that MSCs mediate these comorbidities via a reduction in their native maintenance and repair activities is an intriguing line of inquiry. Here, it is demonstrated that the number of bone marrow-derived MSCs in people with T2DM was reduced compared to that of age-matched control (AMC) donors and that this was due to a specific decrease in the number of MSCs with osteogenic capacity. There were no differences in MSC cell surface phenotype or in MSC expansion, differentiation, or angiogenic or migratory capacity from donors living with T2DM as compared to AMCs. These findings elucidate the basic biology of MSCs and their potential as mediators of diabetic comorbidities, especially osteopathies, and provide insight into donor choice for MSC-based clinical trials. This study suggests that any role of bone marrow MSCs as a mediator of T2DM comorbidity is likely due to a reduction in the osteoprogenitor population size and not due to a permanent alteration to the MSCs’ capacity to maintain tissue homeostasis through expansion and differentiation.
Highlights
Mesenchymal stromal cells (MSCs) are adult- or extraembryonic conceptus-derived multipotent progenitor cells
It was here hypothesized that type 2 diabetes mellitus (T2DM) impacts the bone marrow MSC population, with potential implications for bone homeostasis in humans
This is in line with what has been observed in other complications associated with diabetes mellitus (DM) and in rodent models of T2DM [10,12]
Summary
Mesenchymal stromal cells (MSCs) are adult- or extraembryonic conceptus-derived multipotent progenitor cells. Theorised to play a crucial role in in vivo tissue repair and homeostasis, they have been strictly defined in vitro as having specific properties. These criteria, set by the International Society for Cellular Therapy (ISCT), include the ability to differentiate into osteoblasts, adipocytes and chondrocytes; plastic adherence in cell culture; and the presence and absence of a defined set of surface markers (CD73+, CD90+, CD105+, CD34−, CD45−, CD11b− or CD14−, CD19− or CD79α−, and HLA-DR−) [1]. Shifts in the fate choice of MSCs, reduction in their overall proliferative capacity or in their differentiation to a particular cell type, as well as their role in mediating the activity of other cell populations have been demonstrated to play varying roles in disease progression [3,4,5]
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