title: Effects of anti-β2-glycoprotein I antibody on PlGF, VEGF and sVEGFR1 production from cultured choriocarcinoma cell line.
abstract: OBJECTIVE
  Anti-β2-glycoprotein I (anti-β2-GPI) antibody has been detected in cases of recurrent abortion and intrauterine death. Placenta growth factor (PlGF) and vascular endothelial growth factor (VEGF) are growth factors that accelerate villous proliferation. Soluble VEGF receptor-1 (sVEGFR1) is a soluble receptor for PlGF and suppresses the function of PlGF. In order to study the pathological mechanism of anti-β2-GPI antibody, we evaluated the effects of anti-β2-GPI antibody on PlGF, VEGF and sVEGFR1 production from cultured choriocarcinoma cells.
  
  
  METHODS
  The sera were taken from six anti-β2-GPI antibody-positive and six anti-β2-GPI antibody-negative patients with recurrent miscarriages. Choriocarcinoma cells (JEG-3) were cultured in 24-well plates. After each serum and isolated immunoglobulin G (IgG) were added to the culture medium, the PlGF, VEGF and sVEGFR1 in the culture medium were measured by ELISA 24 h later. When the isolated IgG was added to culture medium, only the levels of PlGF were measured.
  
  
  RESULTS
  The anti-β2-GPI antibody-positive sera and isolated IgG significantly suppressed the production of PlGF from JEG-3 cells more strongly than the anti-β2-GPI antibody-negative sera. The suppressive effects were not changed by serum inactivation. There was no significant difference in the values of the XTT assay and the production of VEGF and sVEGFR1 between the antibody-positive and antibody-negative sera.
  
  
  CONCLUSIONS
  Anti-β2-GPI antibody-positive sera and IgG suppress the production of PlGF from JEG-3 cells. We suggest that the anti-β2-GPI antibodies may suppress PlGF production from trophoblasts and cause the failure of placenta formation and function.
authors.affiliation: Department of Obstetrics and Gynecology, Nihon University School of Medicine, Tokyo, Japan.
authors.forename: Go
authors.initials: G
authors.lastname: Ichikawa
authors.forename: Tatsuo
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Fumihisa
authors.initials: F
authors.lastname: Chishima
authors.forename: Akikazu
authors.initials: A
authors.lastname: Nakamura
authors.forename: Souichirou
authors.initials: S
authors.lastname: Kuno
authors.forename: Takayuki
authors.initials: T
authors.lastname: Murase
authors.forename: Manami
authors.initials: M
authors.lastname: Suzuki
mesh_terms: D000026:Abortion, Habitual / Q000276:immunology* / Q000378:metabolism; D000328:Adult; D001323:Autoantibodies / Q000032:analysis / Q000302:isolation & purification / Q000378:metabolism*; D045744:Cell Line, Tumor; D002822:Choriocarcinoma / Q000378:metabolism; D015536:Down-Regulation; D005260:Female; D006801:Humans; D000072483:Placenta Growth Factor; D011257:Pregnancy Proteins / Q000097:blood / Q000378:metabolism*; D014327:Trophoblasts / Q000378:metabolism*; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000097:blood / Q000378:metabolism*; D042442:Vascular Endothelial Growth Factors / Q000097:blood / Q000378:metabolism*; D055815:Young Adult; D053482:beta 2-Glycoprotein I / Q000037:antagonists & inhibitors* / Q000502:physiology
chemical_list: D001323:Autoantibodies; C000608036:PGF protein, human; D011257:Pregnancy Proteins; D042442:Vascular Endothelial Growth Factors; D053482:beta 2-Glycoprotein I; D000072483:Placenta Growth Factor; C501162:FLT1 protein, human; D040281:Vascular Endothelial Growth Factor Receptor-1