High Glucose Impairs Early and Late Endothelial Progenitor Cells by Modifying Nitric Oxide–Related but Not Oxidative Stress–Mediated Mechanisms

Chen, Yung‐Hsiang; Lin, Shing Jong; Lin, Feng Yen; Wu, Tao Cheng; Tsao, Chen Rong; Huang, Po Hsun; Liu, Po Len; Chen, Yuh‐Lien; Chen, Jaw Wen

doi:10.2337/db06-1103

Cited by 296 publications

(286 citation statements)

References 51 publications

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“…Recently, however, Chen et al (35) demonstrated that adult peripheral blood ECFCs treated with hyperglycemia exhibited enhanced senescence and reduced tube-forming ability in vitro, although the dextrose concentrations required to induce these phenotypes were much higher (20 -30 mmol/l or 360 -540 mg/dl) compared with our studies. The distinction between the degree of hyperglycemia required to induce functional changes in neonatal versus adult ECFCs may reflect important developmental differences that deserve further investigation.…”

Section: Discussioncontrasting

confidence: 91%

In Vitro Hyperglycemia or a Diabetic Intrauterine Environment Reduces Neonatal Endothelial Colony-Forming Cell Numbers and Function

et al. 2008

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OBJECTIVE-Emerging data demonstrate that maternal diabetes has long-term health consequences for offspring, including the development of hypertension. In adults, circulating endothelial progenitor cells (EPCs) participate in vascular repair, and EPC numbers and function inversely correlate with the risk of developing vascular disease. Therefore, our objectives were to determine whether hyperglycemia or exposure to a diabetic intrauterine environment alters EPC function. RESEARCH DESIGN AND METHODS-We used well-established clonogenic endothelial colony-forming cell (ECFC) assays and murine transplantation experiments to examine human vasculogenesis.RESULTS-Both in vitro hyperglycemia and a diabetic intrauterine environment reduced ECFC colony formation, self-renewal capacity, and capillary-like tube formation in matrigel. This cellular phenotype was linked to premature senescence and reduced proliferation. Further, cord blood ECFCs from diabetic pregnancies formed fewer chimeric vessels de novo after transplantation into immunodeficient mice compared with neonatal ECFCs harvested from uncomplicated pregnancies. CONCLUSIONS-Collectively, these data demonstrate that hyperglycemia or exposure to a diabetic intrauterine environment diminishes neonatal ECFC function both in vitro and in vivo, providing potential mechanistic insights into the long-term cardiovascular complications observed in newborns of diabetic pregnancies. Diabetes 57:724-731, 2008

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Section: Discussioncontrasting

confidence: 91%

In Vitro Hyperglycemia or a Diabetic Intrauterine Environment Reduces Neonatal Endothelial Colony-Forming Cell Numbers and Function

et al. 2008

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“…Specifically, diabetes has been shown to be associated with a significant impairment in adaptive vascular growth of both capillarylike tube vessels and collateral vessels [1,2]. Increasing evidence indicates that high glucose and AGEs are the initiating causes of vascular damage in diabetes [3,4], acting on both resident endothelial cells (ECs) and endothelial progenitor cells (EPCs) [5,6]. Although multiple growth factors have been shown to regulate vascular growth, little is known about the complex upstream regulation of gene expression and translation in these settings.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: MIR221/MIR222-driven post-transcriptional regulation of P27KIP1 and P57KIP2 is crucial for high-glucose- and AGE-mediated vascular cell damage

et al. 2011

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Aims/hypothesis MicroRNAs (miRNAs) are a novel group of small non-coding RNAs that regulate gene expression at the post-transcriptional level and act on their target mRNAs in a tissue-and cell-type-specific manner. Herein, the relevance of MIR221/MIR222 in high-glucose-and AGEmediated vascular damage was investigated. Methods Functional studies were performed using human mature endothelial cells and endothelial progenitor cells subjected to high glucose or AGE. Quantitative real-time amplification was performed to analyse MIR221/MIR222 expression in these experimental conditions. Luciferase assay was used to identify MIR221/MIR222 targets. Functional studies were performed in vitro and in vivo in mice using gain-and loss-of-function approaches. Results Using an in vivo mouse model we demonstrated that exposure to AGE and high glucose impaired vessel formation. Moreover, in vitro functional studies revealed that both high glucose and AGE inhibit cell-cycle progression by modulating the expression of P27KIP1 (also known as CDKN1B) and P57KIP2 (also known as CDKN1C), which encode cyclindependent kinase inhibitor 1B (p27, Kip1) (P27KIP1) and cyclin-dependent kinase inhibitor 1C (p57, Kip2) (P57KIP2), respectively. Crucial to AGE-and high-glucose-mediated cellcycle arrest was the downregulation of MIR221/MIR222 expression. Luciferase assay showed that MIR221 and MIR222 specifically bind to the P27KIP1 and P57KIP2 mRNA 3′-untranslated regions, implicating P27KIP1 and P57KIP2 as MIR221/MIR222 targets. These results were confirmed by gainof-function experiments in vitro, and by injecting mice with endothelial cells overexpressing MIR221 and MIR222. Conclusions/interpretation We provide evidence that highglucose-and AGE-induced inhibition of vascular cell proliferation is controlled by MIR221/MIR222-driven posttranscriptional regulation of P27KIP1 and P57KIP2. These data add further insight to the possible contribution of miRNAs in vascular damage mediated by a high-glucose environment.

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“…(Povsic et al 2009). Two distinct EPC populations, including early and late cells, have been identified based on identified differences on outgrowth capability and specific cell surface markers (Chen et al 2007). Recent evidence also unveiled the critical role of Tie-2 receptor on functional and in the development of definitive angiogenesis process (Reinardy et al 2015).…”

Section: Discussionmentioning

confidence: 99%

Angiogenic activity of endothelial progenitor cells through angiopoietin-1 and angiopoietin-2

Siavashi

Sariri

Nassiri

et al. 2016

Animal Cells and Systems

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Angiogenesis is a regulated process involving the proliferation, migration, and remodeling of different cell types particularly mature endothelial cells and recently discovered progenitor cells, named as endothelial progenitor cells (EPCs). Up to now, many attempts have been made to understand the dynamic balance of pro-and anti-angiogenic factors on EPCs on different milieu. It has been accepted that Ang-1, -2 and Tie-1, -2 signaling play a key role on angiogenesis pathways in endothelial lineage cells. In the current experiment, the angiogenic/angiomodulatory potency of Ang-1 and -2 was investigated on isolated EPCs. Freshly isolated EPCs were exposed to different concentrations of Ang-1 and -2 (25 and 50 ng/ml) over a course of 7 and 14 days. Corroborating to our results, a superior effect of Ang-1 on angiogenic properties, including an increased concentration of vascular endothelial growth factor, in vitro tubulogenesis, EPC migratory, Tie-2 expression and clonogenicity, was determined. A large amount of positive mature endothelium markers was achieved in EPCs being-exposed to Ang-1 peptide. Nonetheless, the number of CD133 positive cells increased in the presence of Ang-2. Collectively, we conclude that Ang-1 potentially induces functional and mature vascular-like behavior in EPCs more than Ang-2.ARTICLE HISTORY

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High Glucose Impairs Early and Late Endothelial Progenitor Cells by Modifying Nitric Oxide–Related but Not Oxidative Stress–Mediated Mechanisms

Cited by 296 publications

References 51 publications

In Vitro Hyperglycemia or a Diabetic Intrauterine Environment Reduces Neonatal Endothelial Colony-Forming Cell Numbers and Function

In Vitro Hyperglycemia or a Diabetic Intrauterine Environment Reduces Neonatal Endothelial Colony-Forming Cell Numbers and Function

RETRACTED ARTICLE: MIR221/MIR222-driven post-transcriptional regulation of P27KIP1 and P57KIP2 is crucial for high-glucose- and AGE-mediated vascular cell damage

Angiogenic activity of endothelial progenitor cells through angiopoietin-1 and angiopoietin-2

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