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Phospholipid scramblase 1 expression is enhanced in patients with antiphospholipid syndrome

  • Original Article
  • Published:
Modern Rheumatology

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 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.

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Acknowledgments

The authors thank Miki Aoto for technical support. This work was supported by the Japanese Ministry of Health, Labour and Welfare, the Japanese Ministry of Education, Culture, Sports, Science and Technology (MTX), and the Japanese Society for the promotion of the Science (JSPS). Olga Amengual is funded by JSPS/MEXT (project number 21-40106).

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Correspondence to Tatsuya Atsumi.

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Amengual, O., Atsumi, T., Oku, K. et al. Phospholipid scramblase 1 expression is enhanced in patients with antiphospholipid syndrome. Mod Rheumatol 23, 81–88 (2013). https://doi.org/10.1007/s10165-012-0642-9

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  • DOI: https://doi.org/10.1007/s10165-012-0642-9

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