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Published on: May 31, 2018
Activation of mTOR is involved in anti-β2GPI/β2GPI-induced expression of tissue factor and IL-8 in monocytes
Longfei Xia1, Hong Zhou2, Ting Wang3
1Jiangsu Key Laboratory of Medicine Science and Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu 212013, PR China; Department of Laboratory Medicine, Fourth Hospital of Hebei Medical University, Shi Jiazhuang, Hebei 050000, PR China.
Abstract:
Previous study has demonstrated that activation of the mammalian target of rapamycin (mTOR) pathway in endothelial cells (ECs) results in the formation of chronic vascular lesions associated with antiphospholipid syndrome (APS). In addition, it has been shown that stimulation of monocytes and ECs by antiphospholipid antibodies (aPL) leads to a prothrombotic and proinflammatory state and up-regulated expression of tissue factor (TF) and inflammatory cytokines. However, the role of mTOR in pathogenic mechanisms of APS remains largely unexplored. In the present study, we aimed to investigate whether mTOR was involved in anti-β2GPI/β2GPI complex-induced expression of TF and interleukin-8 (IL-8/CXCL8) in monocytes and explore the relationship among TLR4, mTOR, MAPKs and NF-κB in such a process. The results showed that treatment of anti-β2GPI/β2GPI or APS-IgG/β2GPI complex could markedly induce mTOR activation as well as expression of TF and IL-8 in THP-1 cells or primary monocytes. The mTOR inhibitor rapamycin (100nM) could attenuate the elevated expression of TF and IL-8. In addition, rapamycin could also decrease the phosphorylation of p38, ERK1/2 and NF-κB p65 stimulated by anti-β2GPI/β2GPI or APS-IgG/β2GPI complex, but it had no effect on JNK. Moreover, the anti-β2GPI/β2GPI or APS-IgG/β2GPI complex-induced phosphorylation of mTOR in THP-1 cells was down-regulated through inhibition of p38 (10μM, SB203580) or ERK (5μM, U0126) rather than inhibition of JNK (90nM, SP600125) or NF-κB (20μM, PDTC). Finally, the mTOR activation could also be affected by exposure to TLR4 inhibitor TAK-242 (5μM). Taken together, our results indicated that mTOR was involved in regulating anti-β2GPI/β2GPI-induced expression of TF and IL-8 in monocytes. In addition, the inhibition of mTOR pathway might be beneficial for the prevention and treatment of aPL-mediated thrombosis and inflammation in APS patients.
Insights
The mammalian target of rapamycin (mTOR) pathway is implicated in antiphospholipid syndrome (APS). Inhibiting mTOR reduces tissue factor and IL-8 expression in monocytes, suggesting a therapeutic target for APS-related thrombosis and inflammation.
Area of Science:
- Immunology
- Molecular Biology
- Pathophysiology
Background:
- Antiphospholipid syndrome (APS) is linked to chronic vascular lesions and a prothrombotic state, partly due to antiphospholipid antibodies (aPL) activating endothelial cells and monocytes.
- Previous studies linked mammalian target of rapamycin (mTOR) pathway activation in endothelial cells to APS-related vascular lesions.
- The specific role of mTOR in the pathogenic mechanisms of APS, particularly in monocyte activation, remained largely unexplored.
Purpose of the Study:
- To investigate the involvement of mTOR in the expression of tissue factor (TF) and interleukin-8 (IL-8/CXCL8) in monocytes induced by anti-β2GPI/β2GPI complexes.
- To explore the intricate relationship among Toll-like receptor 4 (TLR4), mTOR, mitogen-activated protein kinases (MAPKs), and nuclear factor-kappa B (NF-κB) in this process.
Main Methods:
- Treatment of THP-1 cells and primary monocytes with anti-β2GPI/β2GPI or APS-IgG/β2GPI complexes.
- Assessment of mTOR activation, TF, and IL-8 expression.
- Utilized mTOR inhibitor rapamycin, specific MAPK inhibitors (p38, ERK1/2, JNK), and a TLR4 inhibitor (TAK-242).
Main Results:
- Anti-β2GPI/β2GPI or APS-IgG/β2GPI complex treatment significantly activated mTOR and increased TF and IL-8 expression in monocytes.
- Rapamycin treatment attenuated the elevated TF and IL-8 expression and decreased the phosphorylation of p38, ERK1/2, and NF-κB p65.
- Inhibition of p38 or ERK, but not JNK or NF-κB, reduced mTOR phosphorylation; TLR4 inhibition also affected mTOR activation.
Conclusions:
- mTOR plays a crucial role in regulating the expression of TF and IL-8 in monocytes induced by anti-β2GPI/β2GPI complexes.
- The findings elucidate a signaling cascade involving TLR4, MAPKs, and mTOR in APS pathogenesis.
- Inhibition of the mTOR pathway presents a potential therapeutic strategy for preventing and treating aPL-mediated thrombosis and inflammation in APS patients.
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