title: [Phosphatase and tensin homolog deleted on chromosome ten/phosphatidyl Inositol 3-kinase/vascular endothelial growth factor signaling pathway changes in the rabbit Kawasaki disease model].
abstract: OBJECTIVE
  To observe the changes of phosphatase and tensin homolog deleted on chromosome ten(PTEN)/ phosphatidyl Inositol 3-kinase(PI3K)/ vascular endothelial growth factor(VEGF)signaling pathway in a rabbit Kawasaki disease model.
  
  
  METHODS
  Model of Kawasaki disease was established in weanling Japanese big-eared rabbits with 10% bovine serum venous injection (2.5 ml/kg, 2 times, and 2 week's interval) through the ear. Twenty four rabbits were divided into 4 groups: control group (without injection of 10% bovine serum albumin, six rabbits); 1 day group (sacrificed a the second day after the establishment of Kawasaki disease models, six rabbits); 7 day group (sacrificed at the seventh day after establishment of Kawasaki disease model, six rabbits); 30 day group (sacrificed at the thirtieth day after establishment of Kawasaki disease model, six rabbits). Pathological analysis was performed on coronary artery tissue samples. The express of PTEN and PI3K were detected by immunohistochemistry. The levels of VEGF and CK were also examined with ELISA and white blood cells were counted.
  
  
  RESULTS
  (1) Coronary artery of model groups was thinner, distorted and had enlarged lumen. (2) PTEN expression in 1 d group, 7 d group and 30 d group were 58.5 ± 12.9, 73.2±9.9 and 109.6 ± 24.4, respectively, significantly higher than in the control group (25.5 ± 6.9, P<0.01 or 0.05). (3) The express of PI3K was significantly upregulated in 1 d group(57.2±11.1)and 7 d group(39.9±4.8) compared to control group(19.1±3.5, P<0.01 or 0.05). The expression level of PI3K in 30 d group was 18.8 ± 7.5, which was similar as control group (P>0.05) and significantly lower than 1 d and 7 d group (both P<0.05). (4) Similarly, the level of VEGF in 1 d group, 7 d group ((89.1 ± 15.5) ng/L, (76.9±9.9) ng/L) were significantly higher while it was significantly lower in 30 d group ((19.8 ± 4.4)ng/L) compared with the control group ((33.9 ± 6.7) ng/L, P<0.01 or 0.05). The level of VEGF in 7 d group was significantly lower than in 1 d group (P<0.05) and the level of VEGF was significantly lower in 30 d group than in 7 d group (P<0.01). (5)Creatine kinase levels were significantly higher in 30 d group than in control group (P<0.05) and there were no significantly different between control group, 1 d group and 7 d group(all P>0.05). (6)White blood cell count were significantly higher in 1 d group, 7 d group and 30 d group than in control group (all P<0.01).
  
  
  CONCLUSIONS
  The level of PTEN/PI3K/VEGF signaling pathway change after establishment of rabbit Kawasaki disease model and the signaling pathway might be involved in this model.
authors.affiliation: Department of Cardiorascular, Children's Hospital of Xuzhou City, Xuzhou 221006, China.
authors.forename: L
authors.initials: L
authors.lastname: Niu
authors.forename: M Y
authors.initials: MY
authors.lastname: Fu
authors.forename: J
authors.initials: J
authors.lastname: Tian
authors.forename: X H
authors.initials: XH
authors.lastname: He
authors.forename: H N
authors.initials: HN
authors.lastname: Zhang
authors.forename: Q W
authors.initials: QW
authors.lastname: Wang
authors.forename: Y
authors.initials: Y
authors.lastname: Wang
authors.forename: C L
authors.initials: CL
authors.lastname: Li
authors.forename: Z Z
authors.initials: ZZ
authors.lastname: Wang
authors.forename: X J
authors.initials: XJ
authors.lastname: An
mesh_terms: D000818:Animals; D002875:Chromosomes; D003331:Coronary Vessels; D008840:Microfilament Proteins; D009080:Mucocutaneous Lymph Node Syndrome; D051059:PTEN Phosphohydrolase; D058539:Phosphatidylinositol 3-Kinase; D019869:Phosphatidylinositol 3-Kinases; D011817:Rabbits; D015398:Signal Transduction; D000070876:Tensins; D042461:Vascular Endothelial Growth Factor A
chemical_list: D008840:Microfilament Proteins; D000070876:Tensins; D042461:Vascular Endothelial Growth Factor A; D019869:Phosphatidylinositol 3-Kinases; D058539:Phosphatidylinositol 3-Kinase; D051059:PTEN Phosphohydrolase