title: Autophagy inhibits endothelial progenitor cells migration via the regulation of MMP2, MMP9 and uPA under normoxia condition.
abstract: OBJECTIVE
  The aim of this study was to explore the role of autophagy on the regulation of endothelial progenitor cells (EPCs) migration under normoxic condition.
  
  
  METHODS
  After EPCs were isolated and characterized in vitro, we employed Atg5 knocking down and rapamycin to monitor the autophagy, and performed wound healing and transwell assay to assess the cell migration. On the mechanism, the expression of matrix metalloproteinases (MMPs) and urokinase type plasminogen activator (uPA) was evaluated.
  
  
  RESULTS
  Atg5 knocking down and rapamycin could respectively inhibit and enhance autophagy, which could result in significantly increased and decreased cell migration in wound healing and transwell assay under normoxic condition. Moreover, Atg5 knocking down could significantly increase the expression of MMP2, MMP9 and uPA in EPCs while rapamycin could decrease the expression of uPA and MMP9. In addition, the mTOR-P70 S6K pathway was also involved in EPCs migration regulation.
  
  
  CONCLUSIONS
  These results demonstrated that autophagy could regulate the EPCs migration through mTOR-P70 S6K pathway, and MMP2, MMP9 and uPA may also involve in the regulation mechanism.
authors.affiliation: Department of Vascular Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
authors.forename: Wen-Dong
authors.initials: WD
authors.lastname: Li
authors.affiliation: Department of Vascular Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
authors.forename: Nan
authors.initials: N
authors.lastname: Hu
authors.affiliation: Department of Vascular Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
authors.forename: Feng-Rui
authors.initials: FR
authors.lastname: Lei
authors.affiliation: Department of Vascular Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
authors.forename: Sen
authors.initials: S
authors.lastname: Wei
authors.affiliation: Department of Vascular Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
authors.forename: Jian-Jie
authors.initials: JJ
authors.lastname: Rong
authors.affiliation: Department of Vascular Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
authors.forename: Hao
authors.initials: H
authors.lastname: Zhuang
authors.affiliation: Department of Vascular Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China. Electronic address: vasculars@126.com.
authors.forename: Xiao-Qiang
authors.initials: XQ
authors.lastname: Li
mesh_terms: D000818:Animals; D001343:Autophagy; D000071187:Autophagy-Related Protein 5; D002465:Cell Movement; D049109:Cell Proliferation; D066026:Endothelial Progenitor Cells / Q000166:cytology*; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism*; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism*; D010100:Oxygen / Q000737:chemistry; D011506:Proteins / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D038762:Ribosomal Protein S6 Kinases, 70-kDa / Q000378:metabolism; D015398:Signal Transduction; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism; D014568:Urokinase-Type Plasminogen Activator / Q000378:metabolism*; D014945:Wound Healing
chemical_list: C545865:Atg5 protein, rat; D000071187:Autophagy-Related Protein 5; D011506:Proteins; C546845:mTOR protein, rat; D038762:Ribosomal Protein S6 Kinases, 70-kDa; D058570:TOR Serine-Threonine Kinases; D014568:Urokinase-Type Plasminogen Activator; D020778:Matrix Metalloproteinase 2; C522363:Mmp2 protein, rat; D020780:Matrix Metalloproteinase 9; C572337:Mmp9 protein, rat; D010100:Oxygen
keywords: Autophagy; Endothelial progenitor cells; Matrix metalloproteinases; Migration