Vol.23 No.1

Original Article

Phospholipid scramblase 1 expression is enhanced in patients with antiphospholipid syndrome

Authors

Olga Amengual¹ , Tatsuya Atsumi¹ , Kenji Oku¹ , Eriko Suzuki¹ , Tetsuya Horita¹ , Shinsuke Yasuda¹ , Takao Koike¹

Received:

28 December 2011

Accepted:

22 March 2012

Published online:

24 April 2012

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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.
Patients and 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 realtime 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.

Key words

Antiphospholipid antibodies - Phosphatidylserine - Tissue factor