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.
journal_name
Int J Mol Scijournal_title
International journal of molecular sciencesauthors
Cassidy FC,Shortiss C,Murphy CG,Kearns SR,Curtin W,De Buitléir C,O'Brien T,Coleman CMdoi
10.3390/ijms21072476subject
Has Abstractpub_date
2020-04-02 00:00:00issue
7issn
1422-0067pii
ijms21072476journal_volume
21pub_type
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