title: Tripterine treatment improves endothelial progenitor cell function via integrin-linked kinase.
abstract: OBJECTIVE
  Atherosclerosis is associated with dysfunction of endothelial progenitor cells (EPCs). Tripterine, a chemical compound derived from the Chinese medicinal plant Tripterygium wilfordii Hook, displays anti-inflammatory properties in several animal models. We hypothesized that tripterine can improve EPC function and thus the efficiency of EPC transplantation.
  
  
  RESULTS
  Tripterine preconditioning (2.5 μM, 4 h) improved EPC proliferation, tube formation, migration, and adhesion, and reduced apoptosis in cells cultured in ox-LDL (200 µg/ml). Tripterine restored integrin-linked kinase (ILK) levels downregulated by ox-LDL in EPCs, suggesting the involvement of the ILK/Akt pathway. Small interfering RNA-mediated depletion of ILK and dominant-negative ILK transduction inhibited the phosphorylation of the ILK downstream signaling targets protein kinase B/Akt and glycogen synthase kinase 3-beta (GSK-3β), and reduced β-catenin and cyclin D1 expression. In atherosclerotic mice injected with green fluorescent protein-labeled EPCs to evaluate EPC function, tripterine decreased aortic lesions and plaque deposition, and injection of tripterine-treated EPCs restored ILK levels.
  
  
  CONCLUSIONS
  The present results suggest that tripterine improves vascular function in atherosclerosis by enhancing EPC function through a mechanism involving the ILK signaling pathway.
authors.forename: Chenhui
authors.initials: C
authors.lastname: Lu
authors.forename: Xixiang
authors.initials: X
authors.lastname: Yu
authors.forename: Keqiang
authors.initials: K
authors.lastname: Zuo
authors.forename: Xiaoping
authors.initials: X
authors.lastname: Zhang
authors.forename: Chuanwu
authors.initials: C
authors.lastname: Cao
authors.forename: Jichong
authors.initials: J
authors.lastname: Xu
authors.forename: Shi
authors.initials: S
authors.lastname: Wang
authors.forename: Tao
authors.initials: T
authors.lastname: Tang
authors.forename: Meng
authors.initials: M
authors.lastname: Ye
authors.forename: Erli
authors.initials: E
authors.lastname: Pei
authors.forename: Georges
authors.initials: G
authors.lastname: Uzan
authors.forename: Kangkang
authors.initials: K
authors.lastname: Zhi
authors.forename: Maoquan
authors.initials: M
authors.lastname: Li
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D050197:Atherosclerosis / Q000378:metabolism / Q000628:therapy*; D002448:Cell Adhesion / Q000187:drug effects; D002465:Cell Movement; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D004195:Disease Models, Animal; D066026:Endothelial Progenitor Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism / Q000637:transplantation; D005786:Gene Expression Regulation / Q000187:drug effects; D008077:Lipoproteins, LDL / Q000009:adverse effects; D051379:Mice; D053978:Pentacyclic Triterpenes; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*; D014315:Triterpenes / Q000494:pharmacology*; D000099200:Scaffold Protein ILK
chemical_list: D000893:Anti-Inflammatory Agents; D008077:Lipoproteins, LDL; D053978:Pentacyclic Triterpenes; D017346:Protein Serine-Threonine Kinases; D014315:Triterpenes; D000099200:Scaffold Protein ILK; C099252:oxidized low density lipoprotein; C050414:celastrol