Comparison of endothelial progenitor cell function in type 2 diabetes with good and poor glycemic control

Churdchomjan, Worachat; Kheolamai, Pakpoom; Manochantr, Sirikul; Tapanadechopone, Pirath; Tantrawatpan, Chairat; U-Pratya, Yaowalak; Issaragrisil, Surapol

doi:10.1186/1472-6823-10-5

Cited by 52 publications

(41 citation statements)

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“…7 Diabetes mellitus adversely affects the function of several adult stem cell populations from noncardiac tissues. [8][9][10][11] Resident CSC abundance has been shown to negatively correlate with type 2 diabetes mellitus. 12 Studies on diabetic bone marrow-derived angiogenic cells have revealed that increased dicarbonyl stress may be causally linked to diabetes mellitus-associated cellular dysfunction.…”

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confidence: 99%

Hyperglycemia Inhibits Cardiac Stem Cell–Mediated Cardiac Repair and Angiogenic Capacity

et al. 2014

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Background-The impact of diabetes mellitus on the cardiac regenerative potential of cardiac stem cells (CSCs) is unknown yet critical, given that individuals with diabetes mellitus may well require CSC therapy in the future. Using human and murine CSCs from diabetic cardiac tissue, we tested the hypothesis that hyperglycemic conditions impair CSC function. Methods and Results-CSCs cultured from the cardiac biopsies of patients with diabetes mellitus (hemoglobin A1c, 10±2%) demonstrated reduced overall cell numbers compared with nondiabetic sourced biopsies (P=0.04). When injected into the infarct border zone of immunodeficient mice 1 week after myocardial infarction, CSCs from patients with diabetes mellitus demonstrated reduced cardiac repair compared with nondiabetic patients. Conditioned medium from CSCs of patients with diabetes mellitus displayed a reduced ability to promote in vitro blood vessel formation (P=0.02). Similarly, conditioned medium from CSCs cultured from the cardiac biopsies of streptozotocin-induced diabetic mice displayed impaired angiogenic capacity (P=0.0008). Somatic gene transfer of the methylglyoxal detoxification enzyme, glyoxalase-1, restored the angiogenic capacity of diabetic CSCs (diabetic transgenic versus nondiabetic transgenic; P=0.8). Culture of nondiabetic murine cardiac biopsies under high (25 mmol/L) glucose conditions reduced CSC yield (P=0.003), impaired angiogenic (P=0.02) and chemotactic (P=0.003) response, and reduced CSC-mediated cardiac repair (P<0.05). Conclusions-Diabetes mellitus reduces the ability of CSCs to repair injured myocardium. Both diabetes mellitus andpreconditioning CSCs in high glucose attenuated the proangiogenic capacity of CSCs. In this study, we have investigated the effects of diabetes mellitus and a hyperglycemic environment on the function of ex vivo proliferated human and murine CSCs. Furthermore, we assessed the ability of GLO-1 overexpression to prevent and reverse hyperglycemia-induced CSC dysfunction. MethodsDetailed experimental methods are available in the online-only Data Supplement. CSC Isolation and CultureHuman CSCs were obtained from left atrial appendages donated by patients (aged 18-80 years) undergoing clinically indicated heart surgery after informed consent. Murine CSCs were obtained from cardiac tissue of wild-type C57Bl/6, C57Bl/6-cKit-EGFP, or C57Bl/6-PEP8-hGlo-1 transgenic mice (aged 2 to 12 months) under isoflurane sedation. CSCs were cultured as described previously. 19,20 Hyperglycemia was induced in C57BL/6 or PEP8-hGlo-1 mice by intraperitoneal injection of streptozotocin (50 mg/kg for 5 days) in 0.05 mol/L sodium citrate. Nondiabetic control mice received equal volumes of 0.05 mol/L sodium citrate. Fasting blood glucose measurements were obtained 10 to 14 days after the fifth streptozotocin injection and again before euthanasia. Mean fasting blood glucose at the time of euthanasia was 29.0±2.3 mmol/L for streptozotocin-injected animals versus 5.6±0.1 mmol/L for controls (P=0.0005). Diabetic Cardiac Explant GLO-1 and...

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Hyperglycemia Inhibits Cardiac Stem Cell–Mediated Cardiac Repair and Angiogenic Capacity

et al. 2014

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“…Further, the number and function of EPCs in patients with good glycemic control were recovered compared with those with poor glycemic control. When glucose was supplemented to in vitro cultures, there was a negative effect on the proliferation and viability of EPCs, in a dose-dependent manner, whereas the enhancement of apoptosis was observed (Churdchomjan et al, 2010). All these deleterious effects were reported to occur due to a direct effect of elevated glucose levels on EPCs , however it was also suggested that hyperglycemia may promote EPCs dysfunction indirectly through the induction of Reactive Oxygen Species (ROS) overproduction and increased oxidative stress (Callaghan et al,.…”

Section: Hyperglycemiamentioning

confidence: 99%

Vasculogenesis in Diabetes-Associated Diseases: Unraveling the Diabetic Paradox

Costa¹

2011

Vasculogenesis and Angiogenesis - From Embryonic Development to Regenerative Medicine

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“…Кардиология чество CD34+/VEGFR2+ клеток было в 2,8 раза больше, чем при декомпенсированном СД2 (HbA 1c =9,2±1,4%) и меньше в 1,5 раза по сравнению с контрольной группой [33]. В нашей работе повы-шение количества ЦПК в крови больных ИБС+СД2 комп./суб-комп.…”

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The influence of concomitant type 2 diabetes mellitus on the number of circulating progenitor cells in patients with ischemiccardiomyopathy

et al. 2011

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Aim. To study effect of concomitant type 2 diabetes mellitus on the number of circulating progenitor cells (CPC) in patients with coronary heart disease(CHD) and postinfarction heart failure (ischemic cardiomyopathy).Methods. The number of CPC (CD34+ cells) was determined by flow cytophotometry in 47 patients with CHD including 14 with CHD + DM2; 12patients without CHD and DM2 made up the control grouP. Enzyme-linked immunosorbent assay was used to measure N-terminal precursor of brainnatriuretic peptide (NT-proBNP), immunoreactive insulin (IRI) and C-peptide levels. Results. The number of CPC in patients with ischemic cardiomyopathy without DM2 was 33.4% greater than in controls. In patients with cardiomyopathyand DM2 the number of CPC depended on the quality of diabetes compensation. It was lowest in case of decompensated DM2 (HbA1c=9.5?1.8%).In patients with compensated/subcompensated DM2 (HbA1c=6.8?0.3%) it was significantly higher than in controls and patients with ischemiccardiomyopathy without DM2 (mean 46.5 (p=0.006) and 40.0% (p=0.02) respectively). Conclusion. The number of CPC in peripheral blood of patients with ischemic cardiomyopathy and DM2 correlated with the level of DM compensation.It was lowest in patients with decompensated DM2 and exceeded the normal number in patients with CHD without DM2. The number of CPC inverselycorrelated with blood glucose level. Positive correlation of CPC number with IRI and C-peptide levels was documented in control subjects and patientswith CHD without DM2.

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Comparison of endothelial progenitor cell function in type 2 diabetes with good and poor glycemic control

Cited by 52 publications

References 43 publications

Hyperglycemia Inhibits Cardiac Stem Cell–Mediated Cardiac Repair and Angiogenic Capacity

Hyperglycemia Inhibits Cardiac Stem Cell–Mediated Cardiac Repair and Angiogenic Capacity

Vasculogenesis in Diabetes-Associated Diseases: Unraveling the Diabetic Paradox

The influence of concomitant type 2 diabetes mellitus on the number of circulating progenitor cells in patients with ischemiccardiomyopathy

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