title: Effect of serum from patients with severe acute pancreatitis on vascular endothelial permeability.
abstract: OBJECTIVE
  This study aimed to investigate the effect of serum taken from patients with severe acute pancreatitis (SAP) on vascular endothelial permeability.
  
  
  METHODS
  The monolayer permeability of endothelial cells (ECs) was assessed. Morphological changes in ECs, induced by serum from patients with SAP were assessed. Expressions of RhoA, myosin light chain (MLC) phosphorylation, and VE-cadherin protein were detected by Western blot.
  
  
  RESULTS
  Compared with the control group, 20% SAP serum significantly increased endothelial monolayer permeability (P < 0.01), markedly induced transcellular F-actin redistribution with stress fiber formation and VE-cadherin derangement with fragmentations located at the cell borders, and increased gaps between ECs. Furthermore, Western blotting showed that SAP serum induced rapid activation of Rho protein, and markedly increased the level of phosphorylated MLC. However, pretreatment with Y-27632 (an inhibitor for Rho kinase) significantly inhibited endothelial hyperpermeability and the morphological changes of F-actin rearrangement and VE-cadherin redistribution. This was associated with a down-regulation of Rho protein expression and a reduction in the level of MLC phosphorylation.
  
  
  CONCLUSIONS
  The SAP serum induces the loss of vascular endothelial monolayer integrity, with endothelial F-actin stress fiber formation and VE-cadherin redistribution. One of the mechanisms for this process involves the activation of the Rho/Rho kinase signaling pathway.
authors.affiliation: Emergency Department, Xin Hua Hospital, China.
authors.forename: Yun-Jiang
authors.initials: YJ
authors.lastname: Zheng
authors.forename: Bin
authors.initials: B
authors.lastname: Zhou
authors.forename: Gang
authors.initials: G
authors.lastname: Ding
authors.forename: Zhan-Chao
authors.initials: ZC
authors.lastname: Wang
authors.forename: Xiao-Qiang
authors.initials: XQ
authors.lastname: Wang
authors.forename: Yi-Lin
authors.initials: YL
authors.lastname: Wang
authors.forename: Yao-Qing
authors.initials: YQ
authors.lastname: Tang
mesh_terms: D000199:Actins / Q000378:metabolism; D000577:Amides / Q000494:pharmacology; D015703:Antigens, CD / Q000378:metabolism; D001381:Azepines / Q000494:pharmacology; D015820:Cadherins / Q000378:metabolism; D002199:Capillary Permeability / Q000187:drug effects / Q000502:physiology*; D016022:Case-Control Studies; D042783:Endothelial Cells / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D061307:Human Umbilical Vein Endothelial Cells; D006801:Humans; D009219:Myosin-Light-Chain Kinase / Q000037:antagonists & inhibitors / Q000378:metabolism; D010195:Pancreatitis / Q000097:blood* / Q000503:physiopathology*; D011725:Pyridines / Q000494:pharmacology; D020742:rhoA GTP-Binding Protein / Q000037:antagonists & inhibitors / Q000378:metabolism; D000099152:Cadherin 5
chemical_list: D000199:Actins; D000577:Amides; D015703:Antigens, CD; D001381:Azepines; D015820:Cadherins; D004791:Enzyme Inhibitors; D009219:Myosin-Light-Chain Kinase; D011725:Pyridines; D020742:rhoA GTP-Binding Protein; D000099152:Cadherin 5; C056218:ML 9; C066737:RHOA protein, human; C108830:Y 27632