Corrigendum to “Effects of homocysteine on number and activity of endothelial progenitor cells from peripheral blood” [J. Mol. Cell. Cardiol. 36 (2004) 233–239]

Chen, J.Z.; Zhu, Jiali; Wang, X.X.; Xie, Xudong; Sun, Jian; Shang, Yunpeng; Guo, Xichao; Dai, Houde; Hu, Shen‐Jiang

doi:10.1016/j.yjmcc.2010.04.003

Cited by 4 publications

(3 citation statements)

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“…EPCs were prepared as described previously. 5) Briefly, mononuclear cells were isolated from peripheral blood 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: Methodsmentioning

confidence: 99%

“…4) In vitro, homocysteine (Hcy) dose-and time-dependently decreases EPC numbers and impairs cell proliferation, migration, and vasculogenesis capacity. 5) Impaired EPC numbers and functional capacity have been identified in a murine model with HHcy. 6) One possible explanation for the reduced capacity of EPCs is increased apoptosis of premature progenitor cells.…”

Section: Homocysteine-induced Caspase-3 Activation By Endoplasmic Retmentioning

confidence: 99%

See 1 more Smart Citation

Homocysteine-Induced Caspase-3 Activation by Endoplasmic Reticulum Stress in Endothelial Progenitor Cells from Patients with Coronary Heart Disease and Healthy Donors

Gong

et al. 2011

Bioscience, Biotechnology, and Biochemistry

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Section: Methodsmentioning

confidence: 99%

Section: Homocysteine-induced Caspase-3 Activation By Endoplasmic Retmentioning

confidence: 99%

Homocysteine-Induced Caspase-3 Activation by Endoplasmic Reticulum Stress in Endothelial Progenitor Cells from Patients with Coronary Heart Disease and Healthy Donors

Gong

et al. 2011

Bioscience, Biotechnology, and Biochemistry

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“…8 Another proatherosclerotic factor, homocysteine, reduces EPC outgrowth in vitro by accelerating the onset of EPC senescence and thereby inhibiting proliferation. 79,80 Hyperhomocysteinemia is commonly observed in several autoimmune diseases. 81 In RA patients, the release of TNF might be pivotal in reducing EPC levels, as corticosteroid treatment normalized EPC levels 44 and infliximab effectively increased levels of these cells.…”

Section: Epc Levels In the Bone Marrowmentioning

confidence: 99%

Endothelial progenitor cell dysfunction in rheumatic disease

Westerweel

Verhaar

2009

Nat Rev Rheumatol

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Rheumatic disease is characterized by inflammation and endothelial dysfunction, which contribute to accelerated atherosclerosis. Circulating endothelial progenitor cells (EPCs) can restore dysfunctional endothelium and thereby protect against atherosclerotic vascular disease. The number and function of EPCs are, however, affected in rheumatic diseases such as psoriatic arthritis, rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, and antineutrophil cytoplasmic autoantibody-associated vasculitis. rheumatic disease is often characterized by decreased numbers, and impaired function, of EPCs, although numbers of these cells might increase during the initial years of systemic sclerosis. Pioneering studies show that EPC dysfunction might be improved with pharmacological treatment. How best to restore EPC function, and whether achieving this aim can prevent long-term cardiovascular complications in rheumatic disease, remain to be established.

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Dual Effects of Cigarette Smoke Extract on Proliferation of Endothelial Progenitor Cells and the Protective Effect of 5-aza-2′-deoxycytidine on EPCs against the Damage Caused by CSE

Chen

et al. 2014

BioMed Research International

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Cigarette smoke is a major public health problem associated with multitude of diseases, including pulmonary and vascular diseases. Endothelial progenitor cells (EPCs) contribute to neovascularization and play an important role in the development of these diseases. The effect of CSE on EPCs is seldom studied. The aim of the current study is to observe the effect of CSE on biological behavior of EPCs and, further, to search for potential candidate agent in protection of proliferation of EPCs against the damage caused by CSE exposure in vitro. Methods. The proliferations of EPCs isolated from bone marrow of C57BL/6J mice were assessed by MTT after incubating the EPCs with a series of concentrations of CSE (1.0%, 2.5%, 5.0%, and 10.0%) for different times (3, 6, and 24 hours) as well as with 1.0% CSE in presence of 5-AZA-CdR for 24 hours. Results. The proliferations of EPCs were significantly enhanced after 3 hours of exposure to concentrations of 1.0% and 2.5% CSE but depressed when exposed to concentrations of 5.0% and 10.0% CSE. Furthermore, the 5-AZA-CdR in concentrations of 2.0 μmol/L and 5.0 μmol/L partly protected against the depression of proliferation of EPCs caused by CSE exposure. Conclusions. The CSE showed dual effects on proliferation of EPCs isolated from mice. The 5-AZA-CdR partly protected the proliferation of EPCs against the damage caused by CSE exposure in vitro, suggesting that DNA methylation may be involved in the dysfunction of EPCs induced by CSE.

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Corrigendum to “Effects of homocysteine on number and activity of endothelial progenitor cells from peripheral blood” [J. Mol. Cell. Cardiol. 36 (2004) 233–239]

Cited by 4 publications

References 0 publications

Homocysteine-Induced Caspase-3 Activation by Endoplasmic Reticulum Stress in Endothelial Progenitor Cells from Patients with Coronary Heart Disease and Healthy Donors

Homocysteine-Induced Caspase-3 Activation by Endoplasmic Reticulum Stress in Endothelial Progenitor Cells from Patients with Coronary Heart Disease and Healthy Donors

Endothelial progenitor cell dysfunction in rheumatic disease

Dual Effects of Cigarette Smoke Extract on Proliferation of Endothelial Progenitor Cells and the Protective Effect of 5-aza-2′-deoxycytidine on EPCs against the Damage Caused by CSE

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