Endothelial Progenitor Cells Are Related to Glycemic Control in Children With Type 1 Diabetes Over Time

Hörtenhuber, Thomas; Rami-Mehar, Birgit; Satler, Miriam; Nagl, Katrin; Höbaus, Clemens; Höllerl, Florian; Koppensteiner, Renate; Schernthaner, Guntram; Schober, Edith; Schernthaner, Gerit-Holger

doi:10.2337/dc12-1206

Cited by 50 publications

(47 citation statements)

References 47 publications

(60 reference statements)

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“…However, this is not always the case. Although some clinical observations suggest a reversibility of diabetes-induced progenitor cell dysfunction, 15,101 preclinical data indicate that progenitor cell deficits may be reversible only in part, after normalization of the glycemic environment. 55 Normalizing glucose in vitro in bone marrow progenitor cell cultures or in vivo in type 1 diabetic mice by insulin treatment reveals these phenomena of partial reversal of function.…”

Section: Diabetic Stem and Progenitor Cell Defects Are Reversible Onlmentioning

confidence: 99%

Progenitor Cell Dysfunctions Underlie Some Diabetic Complications

Rodrigues

Wong

Rennert

et al. 2015

The American Journal of Pathology

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Stem cells and progenitor cells are integral to tissue homeostasis and repair. They contribute to health through their ability to self-renew and commit to specialized effector cells. Recently, defects in a variety of progenitor cell populations have been described in both preclinical and human diabetes. These deficits affect multiple aspects of stem cell biology, including quiescence, renewal, and differentiation, as well as homing, cytokine production, and neovascularization, through mechanisms that are still unclear. More important, stem cell aberrations resulting from diabetes have direct implications on tissue function and seem to persist even after return to normoglycemia. Understanding how diabetes alters stem cell signaling and homeostasis is critical for understanding the complex pathophysiology of many diabetic complications. Moreover, the success of cell-based therapies will depend on a more comprehensive understanding of these deficiencies. This review has three goals: to analyze stem cell pathways dysregulated during diabetes, to highlight the effects of hyperglycemic memory on stem cells, and to define ways of using stem cell therapy to overcome diabetic complications. Diabetes is characterized by insulin resistance and hyperglycemia, and affects a diverse array of cells, leading to a myriad of tissue complications. These include, but are not limited to, cardiac arrest, stroke, nephropathy, retinopathy, and non-traumatic lower limb amputations.1 Results from randomized clinical trials indicate that adequate glycemic control in diabetic patients reduces the risk of developing one or several of these complications. 2e4 The Diabetes Control and Complications Trial reports a reduction in the development or progression of diabetic nephropathy (50% reduction), neuropathy (60% reduction), and retinopathy (76% reduction) after intensive glycemic control. However, 33% of Americans with diabetes remain undiagnosed, approximately 12% of US adults with diabetes exhibit poor glycemic control, and different medical organizations recommend different glycemic targets, increasing the occurrence of diabetic complications.

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Section: Diabetic Stem and Progenitor Cell Defects Are Reversible Onlmentioning

confidence: 99%

Progenitor Cell Dysfunctions Underlie Some Diabetic Complications

Rodrigues

Wong

Rennert

et al. 2015

The American Journal of Pathology

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“…Indeed, the reduction in circulating EPCs seems to correlate with glycemic control or severity of impaired glucose tolerance in subjects with or without established DM, respectively. [14][15][16][17][18][19][20] Similarly, the deleterious effects of hyperglycemia on the number and function of late EPCs have also been reported. Late EPCs were found in an activated state in patients with DM.…”

Section: Yiu and Tse Diabetes Mellitus And Endothelial Progenitor Celmentioning

confidence: 99%

“…Indeed, the severity of hyperglycemia seems to be negatively correlated with EPC number and function in patients with DM. [14][15][16][17][18][19][20] In an animal model of type 1 DM, successful restoration of normoglycemia by islet transplantation increased the number of EPCs and improved their angiogenic function. 66 Currently, there are only limited data on the optimal antidiabetic therapy to reverse EPC dysfunction in DM.…”

Section: Antidiabetic Agentsmentioning

confidence: 99%

Specific Role of Impaired Glucose Metabolism and Diabetes Mellitus in Endothelial Progenitor Cell Characteristics and Function

Yiu

Tse

2014

ATVB

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Abstract-The disease burden of diabetes mellitus (DM) and its associated cardiovascular complications represent a growing and major global health problem. Recent studies suggest that circulating exogenous endothelial progenitor cells (EPCs) play an important role in endothelial repair and neovascularization at sites of injury or ischemia. 1 This has been attributed to the occurrence of endothelial dysfunction that leads to the initiation and progression of atherosclerotic vascular disease 2 and impaired neovascularization after ischemia induced by hyperglycemia. 3,4 In patients with impaired glucose metabolism and DM, the vascular endothelium is challenged by inflammation, reactive oxygen species, and deletion of endothelial nitric oxide synthase (eNOS) with resultant endothelial dysfunction.2,5-7 The depletion and dysfunction of the circulating endothelial progenitor cells (EPCs) are thought to underlie the endothelial dysfunction in DM. In this review, the possible mechanisms, functional consequences, and the potential therapeutic approach for impaired EPCs in DM are discussed. A systematic literature search for full-text papers in the English language was performed using MEDLINE, Embase, and the Cochrane library through to February 2014. In the search phrases used, the following terms were combined with the phrase AND Diabetes: endothelial progenitor cells, cardiovascular disease, myocardial infarction, and stroke.

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“…Diabetes mellitus is characterized by a defective mechanisms of vascular repair [2] caused by an impaired regenerative capacity of EPCs [3]. EPCs reduction may represent one of the mechanisms linking the elevated vascular risk to diabetes mellitus [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Reducing glucose variability with continuous subcutaneous insulin infusion increases endothelial progenitor cells in type 1 diabetes: an observational study

et al. 2015

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Circulating endothelial progenitor cells (EPCs) are involved in the repairing mechanisms of vascular damage. Glucose variability may contribute to the development of chronic vascular complications of diabetes. We evaluated whether reducing glucose variability with continuous subcutaneous insulin infusion (CSII) would increase circulating levels of EPCs in type 1 diabetes. The study population consisted of 106 type 1 diabetic patients: 41 subjects considered eligible for CSII completed a 6-month follow-up. Sixty-five patients on intensified insulin therapy with multiple daily injections served as control group. Seven EPCs phenotypes were assessed by flow cytometry, and glucose variability by mean amplitude of glycemic excursions (MAGE). Both CD34+KDR+ [difference between groups 32.0, 95 % CI (19.6-44.4) number/10(6) cells, P < 0.001] and CD34+KDR+CD133+ [12.5 (5.5-19.5), P < 0.001)] cell count increased at endpoint in the CSII group, associated with a reduction of MAGE [-1.1 (-2.1 to -0.1), P = 0.026]. No changes occurred in the control group. In multivariate analyses, changes in MAGE were independently associated with changes in both CD34+KDR+ (P = 0.019) and CD34+KDR+CD133+ (P = 0.022) cell count. Reducing glucose variability with CSII in type 1 diabetes increases circulating EPCs levels, suggesting a novel mechanism of vascular damage by oscillating glucose.

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Endothelial Progenitor Cells Are Related to Glycemic Control in Children With Type 1 Diabetes Over Time

Cited by 50 publications

References 47 publications

Progenitor Cell Dysfunctions Underlie Some Diabetic Complications

Progenitor Cell Dysfunctions Underlie Some Diabetic Complications

Specific Role of Impaired Glucose Metabolism and Diabetes Mellitus in Endothelial Progenitor Cell Characteristics and Function

Reducing glucose variability with continuous subcutaneous insulin infusion increases endothelial progenitor cells in type 1 diabetes: an observational study

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