Effects of homocysteine on number and activity of endothelial progenitor cells from peripheral blood

Chen, J

doi:10.1016/j.yjmcc.2003.10.005

Cited by 86 publications

(91 citation statements)

References 23 publications

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“…EPCs were isolated and cultured according to previously described techniques [4,8] . Briefly, mononuclear cells (MNCs) were isolated from mouse bone marrow by Ficoll density gradient centrifugation and cultured on human FN-coated dishes in EGM-2 endothelial medium supplemented with EGM-2-MV-SingleQuots and 20% FBS.…”

Section: Isolation and Cultivation Of Epcsmentioning

confidence: 99%

“…After being washed, the cells were reacted with UEA-1 (10 μg/mL) for 1 h. After being stained, samples were viewed with an inverted fluorescent microscope (Olympus). Cells demonstrating double-positive fluorescence were identified as differentiating EPCs [4,8] . To examine the expression of surface markers on EPCs, cells were incubated for 30 min at 4 °C with phycoerythrin (PE)-conjugated anti-mouse VEGFR-2 (eBioscience) or fluorescein isothiocyanate (FITC)-conjugated anti-mouse CD34 and CD133 antibodies (eBioscience).…”

Section: Identification Of Epcsmentioning

confidence: 99%

“…Patients or mice with hyperhomocysteinemia (HHcy) have lower numbers of EPCs with impaired activities [6,7] . Moreover, an in vitro experiment has shown that Hcy decreased the numbers of EPCs and impaired their proliferation, migration, adhesion and in vitro vasculogenesis capacity [8] . However, the underlying mechanisms responsible for the detrimental effects of Hcy on EPCs remain incompletely elucidated.…”

Section: Introductionmentioning

confidence: 99%

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Atorvastatin inhibits homocysteine-induced dysfunction and apoptosis in endothelial progenitor cells

Bao

2010

Acta Pharmacol Sin

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Aim: To investigate the protective effects of atorvastatin on homocysteine (Hcy)-induced dysfunction and apoptosis in endothelial progenitor cells (EPCs) and the possible molecular mechanisms. Methods: EPCs were divided into six groups: Hcy treatment groups (0, 50, and 500 μmol/L) and atorvastatin pretreatment groups (0.1, 1, and 10 μmol/L). EPC proliferation, migration, in vitro vasculogenesis activity, and apoptosis rate were assayed by the MTT assay, modified Boyden chamber assay, in vitro vasculogenesis kit, and AnnexinV-FITC apoptosis detection kit, respectively. The level of reactive oxygen species (ROS) in cells was measured using H 2 DCF-DA as a fluorescence probe. The activity of NADPH oxidase was evaluated with lucigenin-enhanced chemiluminescence. NO in the supernatant was detected by the nitrate reductase assay. The eNOS mRNA expression and p-eNOS, p-Akt, p-p38MAPK protein expression were measured by RT-PCR and Western blotting analysis, respectively. Caspase-3 activity was determined by colorimetric assay. Results: Hcy does-dependently impaired the proliferation, migration and in vitro vasculogenesis capacity of EPCs, induced cell apoptosis, increased ROS accumulation and NADPH oxidase activation, and decreased the secretion of NO compared with the control group (P<0.05 or P<0.01). The detrimental effects of Hcy were attenuated by atorvastatin pretreatment. Furthermore, Hcy caused a significant downregulation of eNOS mRNA, p-eNOS, and p-Akt protein expression as well as an upregulation of p-p38MAPK protein expression and caspase-3 activity. These effects of Hcy on EPCs were reversed by atorvastatin in a does-dependent manner. Conclusion: Atorvastatin inhibited homocysteine-induced dysfunction and apoptosis in endothelial progenitor cells, which may be related to its effects on suppressing oxidative stress, up-regulating Akt/eNOS and down-regulating the p38MAPK/caspase-3 signaling pathway.

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Section: Isolation and Cultivation Of Epcsmentioning

confidence: 99%

Section: Identification Of Epcsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Atorvastatin inhibits homocysteine-induced dysfunction and apoptosis in endothelial progenitor cells

Bao

2010

Acta Pharmacol Sin

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“…7 Decreased EPC levels may lead to impaired capacity to repair endothelium and thus increase the cardiovascular risks associated with endothelial dysfunctions. In vitro and in vivo studies suggested that hyperhomocysteinemia had detrimental effects on EPCs quantitatively and qualitatively through induction of apoptosis or interference with signaling pathways regulating proliferation, migration, adhesion and vasculogenetic capacity of EPC [14,15]. Furthermore, clinical studies demonstrated that EPCs had an inverse relationship with homocysteine levels in patients with ischemic stroke or controls [15,16].…”

Section: Discussionmentioning

confidence: 99%

1.137 Comparison of Endothelial Progenitor Cells in Parkinson's Disease Patients Treated With Levodopa and Levodopa/Comt Inhibitor

Lee¹,

Lee²,

Sohn³

et al. 2012

Parkinsonism & Related Disorders

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Background: Levodopa treatment in Parkinson's disease (PD) increases in serum homocysteine levels due to its metabolism via catechol O-methyltransferase. Endothelial progenitor cells (EPCs) have the capacity to differentiate into mature endothelial cells and are markers for endothelial functions and cardiovascular risks. Along with traditional vascular risk factors, hyperhomocysteinemia is known to decrease the level of EPCs. In the present study, we hypothesized that that levodopa-induced hyperhomocysteinemia leads to a change in EPC levels.

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“…After incubation for 24 h in a CO 2 incubator, the cell were stained with 4 ′ ,6-diamidino-2-phenylindole (1 µg/ ml, Cat No: D9542; Sigma-Aldrich) and counted. All experiments were performed in triplicate (Vasa et al 2001;Chen et al 2004). …”

Section: Migration Assaymentioning

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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Effects of homocysteine on number and activity of endothelial progenitor cells from peripheral blood

Cited by 86 publications

References 23 publications

Atorvastatin inhibits homocysteine-induced dysfunction and apoptosis in endothelial progenitor cells

Atorvastatin inhibits homocysteine-induced dysfunction and apoptosis in endothelial progenitor cells

1.137 Comparison of Endothelial Progenitor Cells in Parkinson's Disease Patients Treated With Levodopa and Levodopa/Comt Inhibitor

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

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