Activation of MAPKs in the anti-β2GPI/β2GPI-induced tissue factor expression through TLR4/IRAKs pathway in THP-1 cells

Zhou, Hong; Chen, Dongdong; Xie, Hong; Xia, Longfei; Wang, Ting; Yuan, Wei; Yan, Jinchuan

doi:10.1016/j.thromres.2012.08.303

Cited by 21 publications

(22 citation statements)

References 43 publications

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“…Consistently, we found that p38MAPK and ERK1/2 were both activated significantly by the anti-b2GPI/b2GPI complex in THP-1 cells. Another MAPK, JUN1/2, was also activated in this process (Zhou et al, 2012). A major discrepancy between the findings reported by Lopez-Pedrera et al (2006) and our results is that we found NF-jB activity can be regulated by several upstream kinases including p38, JNK and ERK (Xia et al, 2013).…”

Section: Open Questionscontrasting

confidence: 99%

“…Meanwhile, TF mRNA and TF activity were also reduced in paclitaxel pretreated cells. Our study also demonstrated that the MAPKs (p38, extracellular signal-regulated kinase [ERK]1/2 and c-Jun N-terminal kinase [JNK]1/2) were the crucial downstream molecules in anti-b2GPI/b2GPI-triggered TLR4 signalling pathways in monocytes (Zhou et al, 2012).…”

Section: Review ª 2013 John Wiley and Sons Ltdmentioning

confidence: 52%

“…Analysis of the fine epitope specificity of b2GPI-dependent aPL is still a limitation in most studies. Most of the experiments involving TLR4 used total IgG or IgM samples isolated from serum or plasma of APS patients containing a variety of different antibodies Mulla et al, 2009;Lambrianides et al, 2010), some studies used affinity-purified anti-b2GPI IgG rather than total IgG Sorice et al, 2007), and others used animal antibodies (Zhou et al, , 2012Allen et al, 2012). It is striking that these polyclonal IgG samples were obtained from very small numbers of individual patients.…”

Section: Open Questionsmentioning

confidence: 99%

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The role of TLR4 in pathophysiology of antiphospholipid syndrome‐associated thrombosis and pregnancy morbidity

et al. 2013

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SummaryThe antiphospholipid syndrome (APS) is an autoimmune disease characterized by the clinical features of recurrent thrombosis in the venous or arterial circulation and fetal losses. Antiphospholipid antibodies (aPL), particularly against the phospholipid binding protein beta-2 glycoprotein I (b2GPI), play an important role in APS pathological mechanisms. aPL can activate intracellular signal transduction in a b2GPI-dependent manner to induce inflammatory responses, and promote hypercoagulable state and recurrent spontaneous abortion when b2GPI is associated with the cell surface receptor. In vivo and in vitro studies show that Annexin A2 (ANXA2) is the high affinity receptor that connects b2GPI to the target cells. However, ANXA2 is not a transmembrane protein and lacks an intracellular signal transduction pathway. Growing evidences suggest that the transmembrane protein toll-like receptor 4 (TLR4) might act as an 'adaptor' for intracellular signal transduction. This review focuses on the role of TLR4 and its signalling pathway in APS pathological mechanisms which will help us better understand the pathological processes of this syndrome.

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Section: Open Questionscontrasting

confidence: 99%

Section: Review ª 2013 John Wiley and Sons Ltdmentioning

confidence: 52%

Section: Open Questionsmentioning

confidence: 99%

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The role of TLR4 in pathophysiology of antiphospholipid syndrome‐associated thrombosis and pregnancy morbidity

et al. 2013

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“…Our results showed that incubation with palmitate (in similar concentrations used by Voss et al 51 ) reduces enteric neuronal survival as seen by reduced peripherin expression, and also increases TLR4 messenger RNA. Our study also confirmed that TLR4 activation, illustrated by the increase of JNK-1 phosphorylation (mitogen-activated protein kinase involved in the TLR4 pathway 53 ), is required for apoptosis in enteric neurons incubated with palmitate because the specific deletion of this receptor ameliorated the increase of cleaved caspase-3 in the neurons. The activation of TLR4 downstream pathways appears to be critical in the palmitate-induced neuronal apoptosis because in vitro treatment with palmitate induced activation of JNK-1 by causing increased phosphorylation of JNK-1, which was associated with increased neuronal apoptosis.…”

Section: Discussionsupporting

confidence: 82%

26 Intestinal Dysbiosis Contributes to the Delayed Gastrointestinal Transit in High Fat Diet Fed Mice

Anitha¹,

Nezami²,

Mwangi³

et al. 2014

Gastroenterology

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“…Lopez-Pedrera et al indicated that tissue factor expression in THP-1 is partially dependent on activation and phosphorylation of MEK-l/ERK signaling pathway after stimulation with aPL (29). Furthermore, Zhou et al demonstrated that MAPKs (including ERK1/2 along with p38 and JNK1/2) were crucial downstream targets of TLR4 signaling pathways in THP-1 and were triggered by a~2GPII~2GPI (30).…”

Section: Fig 1 Quantificat Ion Of Chemokinelcytokine At the Proteinmentioning

confidence: 99%

High Avidity Anti-β2-Glycoprotein i Antibodies Activate Human Coronary Artery Endothelial Cells and Trigger Peripheral Blood Mononuclear Cell Migration

et al. 2013

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Anti-p2-glycoprotein I antibodies (ap2GPI) represent a potential pathogenic candidate for coronary artery diseases. High avidity ap2GPI (HAv ap2GPI) are known to be associated with thrombotic and obstetric manifestations in patients with antiphospholipid syndrome, who are also susceptible to the development of premature atherosclerosis. However, there is little information about how human coronary artery endothelial cells (HCAEC) are affected by HAv ap2GPI. The purpose of our study was to evaluate the pathophysiological effects of HAv ap2GPI on HCAEC and determine their influence on cytokine expression and migration of peripheral blood mononuclear cells. Following the two hit hypothesis, we co-stimulated HAv ap2GPI-treated HCAEC in the presence and absence of the acute phase protein serum amyloid A (SAA). HAv ap2GPI induced in vitro HCAEC dysfunction, through the ERIO/2 signaling pathway, promoted the expression of chemokines (MCP-l, GROa and IL-8) and IL-6, which led to the attraction and migration of peripheral blood mononuclear cells. These effects were potentiated and intensified in conditions with SAA, indicating that HAv ap2GPI, in the presence of physiological concentrations of acute-phase proteins represent pathogenic autoantibodies, which could lead to the development of premature atherosclerosis and/or thrombosis development.

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Activation of MAPKs in the anti-β2GPI/β2GPI-induced tissue factor expression through TLR4/IRAKs pathway in THP-1 cells

Cited by 21 publications

References 43 publications

The role of TLR4 in pathophysiology of antiphospholipid syndrome‐associated thrombosis and pregnancy morbidity

The role of TLR4 in pathophysiology of antiphospholipid syndrome‐associated thrombosis and pregnancy morbidity

26 Intestinal Dysbiosis Contributes to the Delayed Gastrointestinal Transit in High Fat Diet Fed Mice

High Avidity Anti-β2-Glycoprotein i Antibodies Activate Human Coronary Artery Endothelial Cells and Trigger Peripheral Blood Mononuclear Cell Migration

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