title: Increased RhoA/ROK mRNA expression and function in diabetic vein grafts compared with nondiabetic vein grafts and diabetic arterial grafts.
abstract: OBJECTIVE
  Aim of the study was to discuss a new mechanism underlying the poor graft patency of GSV from diabetic patients and provide a rationale for selecting suitable grafts in diabetic patients.
  
  
  METHODS
  The discarded matched RA, IMA, and GSV from 7 diabetics and 7 nondiabetic patients undergoing CABG were collected and tested for their contractile response to phenylephrine (PE) and their relaxation response to fasudil (a inhibitor of Rho-kinase) and used for immunohistochemical and mRNA detection of RhoA/ROK.
  
  
  RESULTS
  The relaxation response to fasudil of GSV taken from diabetic patients was markedly increased but the relaxation response to fasudil of IMA and RA from diabetic patients was not. Immunohistochemistry and mRNA expression of RhoA/ROK was significantly increased in GSV from diabetic patients compared to that of IMA and RA from diabetic patients. RhoA/ROK immunohistochemistry and mRNA expression were significantly increased in GSV from diabetic patients compared with GSV from nondiabetic controls.
  
  
  CONCLUSIONS
  RhoA/ROK expression and function in GSV from diabetic patients is significantly increased compared with IMA and RA from diabetic patients and GSV from nondiabetic patients. This contributes to a higher incidence of atherosclerosis and a lower long-term patency of GSV from diabetic patients.
authors.affiliation: Cardiology Department, Beijing University People's Hospital, Beijing, China. drj2003@sina.com
authors.forename: R
authors.initials: R
authors.lastname: Ding
authors.forename: D Y
authors.initials: DY
authors.lastname: Hu
authors.forename: K
authors.initials: K
authors.lastname: Xia
authors.forename: X C
authors.initials: XC
authors.lastname: Yang
mesh_terms: D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / Q000031:analogs & derivatives / Q000494:pharmacology; D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D001026:Coronary Artery Bypass / Q000009:adverse effects; D003324:Coronary Artery Disease / Q000150:complications / Q000201:enzymology / Q000235:genetics / Q000601:surgery*; D003920:Diabetes Mellitus / Q000201:enzymology* / Q000235:genetics / Q000503:physiopathology; D005260:Female; D015971:Gene Expression Regulation, Enzymologic; D006083:Graft Occlusion, Vascular / Q000201:enzymology / Q000209:etiology; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008323:Mammary Arteries / Q000201:enzymology; D008875:Middle Aged; D010656:Phenylephrine / Q000494:pharmacology; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D012333:RNA, Messenger / Q000032:analysis*; D017534:Radial Artery / Q000201:enzymology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012501:Saphenous Vein / Q000187:drug effects / Q000201:enzymology* / Q000503:physiopathology / Q000637:transplantation*; D014654:Vascular Patency; D014661:Vasoconstriction; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation; D054460:rho-Associated Kinases / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism; D020742:rhoA GTP-Binding Protein / Q000235:genetics* / Q000378:metabolism
chemical_list: D047428:Protein Kinase Inhibitors; D012333:RNA, Messenger; D014662:Vasoconstrictor Agents; C066737:RHOA protein, human; D010656:Phenylephrine; D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; D054460:rho-Associated Kinases; D020742:rhoA GTP-Binding Protein; C049347:fasudil