Article Text


Experimental research
OX40-OX40L interaction targets NFATc1 in ApoE-/- mice during atherogenesis
  1. Jinchuan Yan,
  2. Liangjie Xu,
  3. Chandran Nagaraj,
  4. Bi Tang,
  5. Jie Gong,
  6. Peijing Liu,
  7. Cuiping Wang,
  8. Guanghua Chen
  1. Division of Cardiology, Department of Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, China; Experimental Anaesthesiology, University Clinic of Anaesthesia and Intensive Care Medicine, Medical University of Graz, A-8036 Graz, Austria


Background We have previously reported the emerging role of OX40-OX40L interaction in inflammation and atherosclerosis. However, the mechanism of OX40-OX40L interaction contribution towards pathogenesis has been poorly understood.

Aim To investigate the effect of OX40-OX40L interaction on the nuclear factor of activated T cells c1(NFATc1) in ApoE-/- mice. Atherosclerotic plaque was induced by rapid perivascular carotid collar placement in ApoE-/- mice. The expression of OX40, OX40L and NFATc1 in lymphocytes was measured by Real Time PCR (RT-PCR) and flow cytometry (FCM), respectively. The presence of NFATc1 in the atherosclerotic plaque was detected by immunohistochemistry. The level of IL-4 was measured by ELISA. We found that the expression of NFATc1 was significantly elevated both in atherosclerotic lesion and in leukocytes from ApoE-/- mice. In vitro, after stimulating OX40-OX40L interaction, the expression level of NFATc1 mRNA and protein was significantly increased in lymphocytes, while anti-OX40LmAb significantly suppressed the expression of NFATc1 in leukocytes, Moreover substantially elevated level of IL-4 was induced by anti-OX40 mAb, while NFATc1 inhibitor markedly suppressed production of IL-4. The current study suggested that OX40-OX40L interaction regulates the expression of NFATc1, which may play a critical role in atherosclerotic plaque formation, which might also have implications with pathophysiology of atherosclerosis.

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