title: [Vascular endothelial injury induced by anti-endothelial cell antibody in allogeneic hematopoietic stem cell transplantation].
abstract: OBJECTIVE
  To clarify the role of endothelial cells (ECs) injury induced by anti-endothelial cell antibody (AECA) in allogeneic hematopoietic stem cell transplantation (allo-HSCT).
  
  
  METHODS
  Serum immunoglobulin (IgG) from allo-HSCT recipients were purified and incubated with human umbilical vein vascular endothelium (HUVEC) in vitro, then the functional changes and cell apoptosis were tested.
  
  
  RESULTS
  After incubation with AECA positive IgG, soluble adhesion molecules significantly elevated in culture supernatant. When concentration of IgG was 160, 320, and 640 μg/ml, concentrations of soluble intercellular adhesion molecule-1 in supernatant were statistically higher in AECA positive groups [(117.10 ± 12.82) vs (78.17 ± 4.90) pg/ml, (151.30 ± 15.35) vs (89.46 ± 6.02) pg/ml, (239.00 ± 32.53) vs (127.80 ± 13.86) pg/ml, P<0.01)]. When concentration of IgG was 40, 80, 160, 320, and 640 μg/ml, concentrations of soluble vascular cell adhesion molecule-1 in supernatant were also statistically higher in AECA positive groups [(38.51 ± 3.76) vs (24.78 ± 2.59) pg/ml, (61.34 ± 6.99) vs (38.20 ± 3.17) pg/ml, (135.60 ± 24.46) vs (63.73 ± 5.08) pg/ml, (221.30 ± 29.40) vs (112.80 ± 8.91) pg/ml, (420.90 ± 31.70) vs (224.40 ± 20.79) pg/ml, P<0.01]. Clotting activity factors also elevated in culture supernatant after incubation with AECA positive IgG. When concentration of IgG was 80, 160, 320, and 640 μg/ml, concentrations of von Willebrand factor were statistically higher in AECA positive groups [(19.51 ± 0.72) vs (17.17 ± 0.60) ng/ml, P=0.0193; (22.97 ± 1.18) vs (18.27 ± 0.61) ng/ml, (26.40 ± 1.54) vs (19.53 ± 0.70) ng/ml, (34.35 ± 1.60) vs (23.81 ± 0.92) ng/ml, P<0.01]. When concentration of IgG was 320 and 640 μg/ml, concentrations of thrombomodulin were statistically higher in AECA positive groups [(57.50 ± 4.50) vs (40.31 ± 4.39) pg/ml, P=0.0132; (59.18 ± 4.11) vs (38.84 ± 5.16) pg/ml, P<0.01]. However, inflammatory factors (IL-1β, IL-6, IL-8 and ANG2) were not statistically different in AECA positive and negative groups (P>0.05). Moreover, IgG from AECA positive samples did not change the proliferation or cell apoptosis.
  
  
  CONCLUSIONS
  AECA from allo-HSCT recipients dysregulates ECs' function in vitro, but do not induce apoptosis, which is valuable in the pathophysiology of graft-versus-host disease (GVHD) and other complications after allo-HSCT.
authors.affiliation: Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences, Tianjin　300020, China.
authors.forename: Jianfeng
authors.initials: J
authors.lastname: Yao
authors.affiliation: Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences, Tianjin　300020, China.
authors.forename: Axia
authors.initials: A
authors.lastname: Song
authors.affiliation: Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences, Tianjin　300020, China.
authors.forename: Zheng
authors.initials: Z
authors.lastname: Ruan
authors.affiliation: Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences, Tianjin　300020, China.
authors.forename: Lukun
authors.initials: L
authors.lastname: Zhou
authors.affiliation: Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences, Tianjin　300020, China.
authors.forename: Peng
authors.initials: P
authors.lastname: Liu
authors.affiliation: Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences, Tianjin　300020, China.
authors.forename: Haiyan
authors.initials: H
authors.lastname: Zhu
authors.affiliation: Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences, Tianjin　300020, China.
authors.forename: Haiyan
authors.initials: H
authors.lastname: Gong
authors.affiliation: Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences, Tianjin　300020, China.
authors.forename: Shuxu
authors.initials: S
authors.lastname: Dong
authors.affiliation: Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences, Tianjin　300020, China.
authors.forename: Yuanfu
authors.initials: Y
authors.lastname: Xu
authors.affiliation: Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences, Tianjin　300020, China.
authors.forename: Erlie
authors.initials: E
authors.lastname: Jiang
authors.affiliation: Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences, Tianjin　300020, China.
authors.forename: Aiming
authors.initials: A
authors.lastname: Pang
authors.affiliation: Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences, Tianjin　300020, China.
authors.forename: Sizhou
authors.initials: S
authors.lastname: Feng
authors.affiliation: Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences, Tianjin　300020, China.
authors.forename: Mingzhe
authors.initials: M
authors.lastname: Han
mesh_terms: D064591:Allografts; D001323:Autoantibodies; D042783:Endothelial Cells; D004730:Endothelium, Vascular; D006086:Graft vs Host Disease; D018380:Hematopoietic Stem Cell Transplantation; D006801:Humans; D018799:Intercellular Adhesion Molecule-1; D015850:Interleukin-6; D014471:Umbilical Veins; D014841:von Willebrand Factor
chemical_list: D001323:Autoantibodies; C508600:IL6 protein, human; D015850:Interleukin-6; C087589:anti-endothelial cell antibody; D014841:von Willebrand Factor; D018799:Intercellular Adhesion Molecule-1