期刊
DIABETES
卷 63, 期 9, 页码 3047-3056出版社
AMER DIABETES ASSOC
DOI: 10.2337/db13-1366
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资金
- NIA NIH HHS [R01 AG025016] Funding Source: Medline
- NIDDK NIH HHS [R01 DK074095] Funding Source: Medline
- NLM NIH HHS [T15 LM007033] Funding Source: Medline
Diabetic vascular pathology is largely attributable to impairments in tissue recovery from hypoxia. Circulating progenitor cells have been postulated to play a role in ischemic recovery, and deficiencies in these cells have been well described in diabetic patients. Here, we examine bone marrow-derived mesenchymal progenitor cells (BM-MPCs) that have previously been shown to be important for new blood vessel formation and demonstrate significant deficits in the context of diabetes. Further, we determine that this dysfunction is attributable to intrinsic defects in diabetic BM-MPCs that are not correctable by restoring glucose homeostasis. We identify two transcriptionally distinct subpopulations that are selectively depleted by both type 1 and type 2 diabetes, and these subpopulations have provasculogenic expression profiles, suggesting that they are vascular progenitor cells. These results suggest that the clinically observed deficits in progenitor cells may be attributable to selective and irreversible depletion of progenitor cell subsets in patients with diabetes.
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