Proteomic analysis of oxidative modification in endothelial colony-forming cells treated by hydrogen peroxide

Wei, Jun; Liu, Ying; Chen, Ming; Sun, Chaoyang; Li, Dawei; Liu, Zhi‐Qiang; Hu, Linsen

doi:10.3892/ijmm.2012.944

Cited by 3 publications

(2 citation statements)

References 48 publications

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“…Various cell activities, including migration, morphological changes and polarity formation are regulated by actin filament dynamics, including actin filament disassembly, severing and reorganization ( 47 , 48 ). Previous studies have demonstrated that actin dysfunction results in impaired ECFC functions, including tubule formation ( 22 , 49 ). Annexin A2 is crucial in actin cytoskeletal rearrangements by binding the regions of free-barbed ends ( 50 ).…”

Section: Discussionmentioning

confidence: 99%

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Atorvastatin protects endothelial colony-forming cells against H2O2-induced oxidative damage by regulating the expression of annexin A2

Wang

et al. 2015

Molecular Medicine Reports

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Endothelial dysfunction and injury are central events in the pathogenesis of ischemic vascular disorders. Endothelial progenitor cells (EPCs) are mobilized from the bone marrow into the peripheral circulation, where they locate to sites of injured endothelium and are involved in endothelial repair and vascular regeneration. During these processes, EPCs are exposed to oxidative stress, a crucial pathological condition, which occurs during vascular injury and limits the efficacy of EPCs in the repair of injured endothelium. Statins are effective inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase, and are commonly used to manage and prevent ischemic vascular disease by reducing plasma cholesterol levels. In addition to lowering cholesterol, statins have also been reported to exert pleiotropic actions, including anti-inflammatory and anti-oxidative activities. The present study aimed to investigate the ability of atorvastatin to protect endothelial colony-forming cells (ECFCs), a homogeneous subtype of EPCs, from hydrogen peroxide (H2O2)-induced oxidative damage, and to determine the mechanism underlying this protective action. MTT assay, acridine orange/ethidium bromide staining, reactive oxygen species assay, western blot analysis and tube formation assay were employed. The results demonstrated that H2O2 induced cell death and decreased the tube-forming ability of the ECFCs, in a concentration-dependent manner; however, these effects were partially attenuated following administration of atorvastatin. The reversion of the quantitative and qualitative impairment of the H2O2-treated ECFCs appeared to be mediated by the regulation of annexin A2, as the expression levels of annexin A2 were decreased following treatment with H2O2 and increased following treatment with atorvastatin. These results indicated that annexin A2 may be involved in the H2O2-induced damage of ECFCs, and in the protective activities of atorvastatin in response to oxidative stress.

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Section: Discussionmentioning

confidence: 99%

“…The tube-forming capacity of ECFCs was measured using a Matrigel assay, as previously described ( 22 , 23 ). Briefly, following treatment, the ECFCs were trypsinized and seeded at a density of 3×10 4 cells/cm 2 onto 96-well plates, which were pre-coated with 50 µ l Matrigel™ (BD Biosciences), and incubated for 24 h at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Atorvastatin protects endothelial colony-forming cells against H2O2-induced oxidative damage by regulating the expression of annexin A2

Wang

et al. 2015

Molecular Medicine Reports

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Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells

et al. 2015

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Diabetes mellitus is a heterogeneous, multifactorial, chronic disease characterized by hyperglycemia owing to insulin insufficiency and insulin resistance (IR). Recent epidemiological studies showed that the diabetes epidemic affects 382 million people worldwide in 2013, and this figure is expected to be 600 million people by 2035. Diabetes is associated with microvascular and macrovascular complications resulting in accelerated endothelial dysfunction (ED), atherosclerosis, and cardiovascular disease (CVD). Unfortunately, the complex pathophysiology of diabetic cardiovascular damage is not fully understood. Therefore, there is a clear need to better understand the molecular pathophysiology of ED in diabetes, and consequently, better treatment options and novel efficacious therapies could be identified. In the light of recent extensive research, we re-investigate the association between diabetes-associated metabolic disturbances (IR, subclinical inflammation, dyslipidemia, hyperglycemia, dysregulated production of adipokines, defective incretin and gut hormones production/action, and oxidative stress) and ED, focusing on oxidative stress and endothelial progenitor cells (EPCs). In addition, we re-emphasize that oxidative stress is the final common pathway that transduces signals from other conditions-either directly or indirectly-leading to ED and CVD.

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Enhancing endothelial colony-forming cells for treating diabetic vascular complications: challenges and clinical prospects

Liu,

Lyons,

Ayu

et al. 2024

Front. Endocrinol.

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Diabetes mellitus (DM) is a metabolic disease characterized by hyperglycemia, leading to various vascular complications. Accumulating evidence indicates that endothelial colony-forming cells (ECFCs) have attractive prospects for repairing and restoring blood vessels. Thus, ECFCs may be a novel therapeutic option for diabetic patients with vascular complications who require revascularization therapy. However, it has been reported that the function of ECFCs is impaired in DM, which poses challenges for the autologous transplantation of ECFCs. In this review, we summarize the molecular mechanisms that may be responsible for ECFC dysfunction and discuss potential strategies for improving the therapeutic efficacy of ECFCs derived from patients with DM. Finally, we discuss barriers to the use of ECFCs in human studies in light of the fact that there are no published reports using these cells in humans.

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Proteomic analysis of oxidative modification in endothelial colony-forming cells treated by hydrogen peroxide

Cited by 3 publications

References 48 publications

Atorvastatin protects endothelial colony-forming cells against H2O2-induced oxidative damage by regulating the expression of annexin A2

Atorvastatin protects endothelial colony-forming cells against H2O2-induced oxidative damage by regulating the expression of annexin A2

Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells

Enhancing endothelial colony-forming cells for treating diabetic vascular complications: challenges and clinical prospects

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