Type 1 diabetes was associated with a 44% reduction in cultured endothelial progenitor cells compared to matched controls (P<0.001), with functional impairment in angiogenesis assays.
Case-Control
Effect estimate: 44% lower
p-value: p=<0.001
Type 1 diabetes is associated with reduced vascular repair, as indicated by impaired wound healing and reduced collateral formation in ischemia. Recently, endothelial progenitor cells (EPCs) have been identified as important regulators of these processes. We therefore explored the concept that EPCs are dysfunctional in diabetes. The number of EPCs obtained from type 1 diabetic patients in culture was 44% lower compared with age- and sex-matched control subjects (P < 0.001). This reduction was inversely related to levels of HbA(1c) (R = -0.68, P = 0.01). In addition, we demonstrated that patient EPCs were also impaired in function using an in vitro angiogenesis assay. Conditioned media from patient EPCs were significantly reduced in their capacity to support endothelial tube formation in comparison to control EPCs. Therefore, despite culturing the EPCs under normoglycemic conditions, functional differences between patient and control EPCs were maintained. Our findings demonstrate that adverse metabolic stress factors in type 1 diabetes are associated with reduced EPC numbers and angiogenicity. We hypothesize that EPC dysfunction contributes to the pathogenesis of vascular complications in type 1 diabetes.
Loomans et al. (Thu,) conducted a case-control in Type 1 diabetes. Type 1 diabetes vs. Age- and sex-matched control subjects was evaluated on Number of endothelial progenitor cells (EPCs) in culture (44% lower, p=<0.001). Type 1 diabetes was associated with a 44% reduction in cultured endothelial progenitor cells compared to matched controls (P<0.001), with functional impairment in angiogenesis assays.