title: Effects of lycopene on number and function of human peripheral blood endothelial progenitor cells cultivated with high glucose.
abstract: OBJECTIVE
  The objectives of this study were to investigate the effects of lycopene on the migration, adhesion, tube formation capacity, and p38 mitogen-activated protein kinase (p38 MAPK) activity of endothelial progenitor cells (EPCs) cultivated with high glucose (HG) and as well as explore the mechanism behind the protective effects of lycopene on peripheral blood EPCs.
  
  
  METHODS
  Mononuclear cells were isolated from human peripheral blood by Ficoll density gradient centrifugation. EPCs were identified after induction of cellular differentiation. Third generation EPCs were incubated with HG (33 mmol/L) or 10, 30, and 50 µg/mL of lycopene plus HG. MTT assay and flow cytometry were performed to assess proliferation and apoptosis of EPCs. EPC migration was assessed by MTT assay with a modified boyden chamber. Adhesion assay was performed by replating EPCs on fibronectin-coated dishes, after which adherent cells were counted. In vitro vasculogenesis activity was assayed by Madrigal network formation assay. Western blotting was performed to analyze protein expression of both phosphorylated and non-phosphorylated p38 MAPK.
  
  
  RESULTS
  The proliferation, migration, adhesion, and in vitro vasculogenesis capacity of EPCs treated with 10, 30, and 50 µg/mL of lycopene plus HG were all significantly higher comapred to the HG group (P < 0.05). Rates of apoptosis were also significantly lower than that of the HG group. Moreover, lycopene blocked phosphorylation of p38 MAPK in EPCs (P < 0.05). To confirm the causal relationship between MAPK inhibition and the protective effects of lycopene against HG-induced cellular injury, we treated cells with SB203580, a phosphorylation inhibitor. The inhibitor significantly inhibited HG-induced EPC injury.
  
  
  CONCLUSIONS
  Lycopene promotes proliferation, migration, adhesion, and in vitro vasculogenesis capacity as well as reduces apoptosis of EPCs. Further, the underlying molecular mechanism of the protective effects of lycopene against HG-induced EPC injury may involve the p38 MAPK signal transduction pathway. Specifically, lycopene was shown to inhibit HG-induced EPC injury by inhibiting p38 MAPKs.
authors.affiliation: Department of Clinical Nutrition, Shenzhen Traditional Chinese Medicine Hospital, China.
authors.forename: Yao-Chi
authors.initials: YC
authors.lastname: Zeng
authors.affiliation: Department of Central Laboratory, Shenzhen Traditional Chinese Medicine Hospital, China.
authors.forename: Gui-Ping
authors.initials: GP
authors.lastname: Mu
authors.affiliation: Department of Health Education, Shenzhen Traditional Chinese Medicine Hospital, China.
authors.forename: Shu-Fen
authors.initials: SF
authors.lastname: Huang
authors.affiliation: Department of Clinical Laboratory, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033, China.
authors.forename: Xue-Hui
authors.initials: XH
authors.lastname: Zeng
authors.affiliation: Department of Cardiovascular Medicine, Shenzhen Traditional Chinese Medicine Hospital, China.
authors.forename: Hong
authors.initials: H
authors.lastname: Cheng
authors.affiliation: Department of Clinical Laboratory, Shenzhen Traditional Chinese Medicine Hospital, Shenzhen, 518033, China.
authors.forename: Zhong-Xin
authors.initials: ZX
authors.lastname: Li
keywords: Lycopene; curve fitting; endothelial progenitor cells; high glucose; p38 MAPK
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