title: Phospholipid scramblase 1 expression is enhanced in patients with antiphospholipid syndrome.
abstract: OBJECTIVE
  Thrombus formation is the key event of vascular manifestations in antiphospholipid syndrome (APS). Phosphatidylserine (PS) is normally sequestered in the inner leaflet of cell membranes. Externalization of PS occurs during cell activation and is essential for promoting blood coagulation and for the binding of antiphospholipid antibodies (aPL) to cells. One of the molecules involved in PS externalization is phospholipid scramblase 1 (PLSCR1). We evaluated PLSCR1 expression on monocytes from APS patients and analyzed the in vitro effect of monoclonal aPL on PLSCR1 expression.
  
  
  METHODS
  Forty patients with APS were investigated. In vitro experiments were performed in monocyte cell lines incubated with monoclonal aPL. PLSCR1 expression was determined by quantitative real-time polymerase chain reactions. PS exposure on CD14(+) cell surface was analyzed by flow cytometry.
  
  
  RESULTS
  Levels of full-length PLSCR1 messenger RNA (mRNA) were significantly increased in APS patients compared with healthy controls (2.4 ± 1.2 vs. 1.3 ± 0.4, respectively, p < 0.001). In cultured monocytes, interferon alpha enhanced tissue-factor expression mediated by β2-glycoprotein-I-dependent monoclonal anticardiolipin antibody.
  
  
  CONCLUSIONS
  Monocytes in APS patients had increased PLSCR1 mRNA expression.
authors.affiliation: Department of Medicine II, Hokkaido University Graduate School of Medicine, N15 W7, Kita-ku, Sapporo, 060-8638, Japan.
authors.forename: Olga
authors.initials: O
authors.lastname: Amengual
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Atsumi
authors.forename: Kenji
authors.initials: K
authors.lastname: Oku
authors.forename: Eriko
authors.initials: E
authors.lastname: Suzuki
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Horita
authors.forename: Shinsuke
authors.initials: S
authors.lastname: Yasuda
authors.forename: Takao
authors.initials: T
authors.lastname: Koike
mesh_terms: D000328:Adult; D000368:Aged; D017153:Antibodies, Anticardiolipin / Q000494:pharmacology; D017152:Antibodies, Antiphospholipid / Q000494:pharmacology; D016736:Antiphospholipid Syndrome / Q000150:complications / Q000201:enzymology* / Q000235:genetics; D002460:Cell Line; D004357:Drug Synergism; D005260:Female; D005434:Flow Cytometry; D015971:Gene Expression Regulation, Enzymologic; D006801:Humans; D016130:Immunophenotyping; D016898:Interferon-alpha / Q000494:pharmacology; D018950:Lipopolysaccharide Receptors / Q000276:immunology / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects / Q000201:enzymology; D010718:Phosphatidylserines / Q000378:metabolism; D049294:Phospholipid Transfer Proteins / Q000235:genetics* / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D013927:Thrombosis / Q000150:complications / Q000201:enzymology* / Q000235:genetics
chemical_list: D017153:Antibodies, Anticardiolipin; D017152:Antibodies, Antiphospholipid; D016898:Interferon-alpha; D018950:Lipopolysaccharide Receptors; C493422:PLSCR1 protein, human; D010718:Phosphatidylserines; D049294:Phospholipid Transfer Proteins; D012333:RNA, Messenger