Activation of the canonical Wnt/β-catenin pathway enhances monocyte adhesion to endothelial cells

Lee, Dong Kun; Grantham, R. Nathan; Trachte, Aaron L.; Mannion, John D.; Wilson, Colleen L.

doi:10.1016/j.bbrc.2006.06.082

Cited by 62 publications

(38 citation statements)

References 40 publications

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“…Finally, over-expression of GSK-3 significantly decreases TNF-α expression in lung and heart tissue (Vines et al, 2006). Other reports suggest that LiCl enhances monocyte adhesion to endothelial cells by activating the Wnt/beta-catenin pathway without changing adhesion molecule expression levels (Lee et al, 2006). The differences between other reports and our study may lie in the type of endothelial cells and stimuli (e.g., TNF-α, IL-1, palmitate) used.…”

Section: Discussioncontrasting

confidence: 82%

Atherosclerosis induced by a high-fat diet is alleviated by lithium chloride via reduction of VCAM expression in ApoE-deficient mice

Choi¹,

Jang²,

Kang³

et al. 2010

Vascular Pharmacology

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Section: Discussioncontrasting

confidence: 82%

Atherosclerosis induced by a high-fat diet is alleviated by lithium chloride via reduction of VCAM expression in ApoE-deficient mice

Choi¹,

Jang²,

Kang³

et al. 2010

Vascular Pharmacology

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“…During the pathogenic process of atherosclerosis, monocytes and other immune cells adhere to endothelial cells of the blood wall. The adhesion, together with inflammatory cytokines such as TNF-a, promotes the migration and proliferation of vascular smooth-muscle cells and the formation of extracellular matrix, which contributes to disease development and progression (Sneddon et al, 2006) The adhesion of monocytes to endothelial cells is likely mediated by intercellular adhesion molecules, such as ICAM-1 and VCAM (Lee et al, 2006). The expression of ICAM-1 can be induced by TNF-a on endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

S‐Allyl‐L‐Cysteine Sulfoxide Inhibits Tumor Necrosis Factor‐Alpha Induced Monocyte Adhesion and Intercellular Cell Adhesion Molecule‐1 Expression in Human Umbilical Vein Endothelial Cells

Chai

et al. 2010

The Anatomical Record

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Garlic and its water-soluble allyl sulfur-containing compound, S-Allyl-Lcysteine Sulfoxide (ACSO), have shown antioxidant and anti-inflammatory activities, inhibiting the development of atherosclerosis. However, little is known about the mechanism(s) underlying the therapeutic effect of ACSO in inhibiting the formation of atherosclerostic lesion. This study aimed to investigate whether ACSO could modulate tumor necrosis factor-alpha (TNF-a)-induced expression of intercellular cell adhesion molecule-1, monocyte adhesion and TNF-a-mediated signaling in human umbilical vein endothelial cells. While TNF-a promoted the intercellular cell adhesion molecule-1 mRNA transcription in a dose-and time-dependent manner, ACSO treatment significantly reduced the levels of TNF-a-induced intercellular cell adhesion molecule-1 mRNA transcripts (P < 0.01). Furthermore, ACSO dramatically inhibited TNF-a triggered adhesion of THP-1 monocytes to endothelial cells and porcine coronary artery rings. Moreover, ACSO mitigated TNF-a induced depolarization of mitochondrial membrane potential and overproduction of superoxide anion, associated with the inhibition of NOX4, a subunit of nicotinamide adenine dinucleotide phosphate-oxidase, mRNA transcription. In addition, ACSO also inhibited TNF-a-induced phosphorylation of JNK, ERK1/2 and IjB, but not p38. Apparently, ACSO inhibited proinflammatory cytokine-induced adhesion of monocytes to endothelial cells by inhibiting the mitogen-activated protein kinase signaling and related intercellular cell adhesion molecule-1 expression, maintaining mitochondrial membrane potential, and suppressing the overproduction of superoxide anion in endothelial cells. Therefore, our findings may provide new insights into ACSO on controlling TNF-a-mediated inflammation and vascular disease. Anat Rec, 293:421-430, 2010. V V C 2010 Wiley-Liss, Inc.

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“…This suggests a role for canonical Wnt signaling in the onset of endothelial activation/dysfunction at sites with altered shear stress and thereby contributing to atherogenesis. In addition, in vitro data demonstrated enhanced monocyte adhesion to endothelial cells by activation of the Wnt/β-catenin pathway without altering expression levels of adhesion molecules (131). Once in the intima, monocytes differentiate to macrophages.…”

Section: Wnt Signaling In Endothelial Dysfunction and Inflammationmentioning

confidence: 97%

Wnt Signaling in Cardiac Disease

Hermans

Blankesteijn

2015

Comprehensive Physiology

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Wnt signaling encompasses multiple and complex signaling cascades and is involved in many developmental processes such as tissue patterning, cell fate specification, and control of cell division. Consequently, accurate regulation of signaling activities is essential for proper embryonic development. Wnt signaling is mostly silent in the healthy adult organs but a reactivation of Wnt signaling is generally observed under pathological conditions. This has generated increasing interest in this pathway from a therapeutic point of view. In this review article, the involvement of Wnt signaling in cardiovascular development will be outlined, followed by its implication in myocardial infarct healing, cardiac hypertrophy, heart failure, arrhythmias, and atherosclerosis. The initial experiments not always offer consensus on the effects of activation or inactivation of the pathway, which may be attributed to (i) the type of cardiac disease, (ii) timing of the intervention, and (iii) type of cells that are targeted. Therefore, more research is needed to determine the exact implication of Wnt signaling in the conditions mentioned above to exploit it as a powerful therapeutic target.

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Activation of the canonical Wnt/β-catenin pathway enhances monocyte adhesion to endothelial cells

Cited by 62 publications

References 40 publications

Atherosclerosis induced by a high-fat diet is alleviated by lithium chloride via reduction of VCAM expression in ApoE-deficient mice

Atherosclerosis induced by a high-fat diet is alleviated by lithium chloride via reduction of VCAM expression in ApoE-deficient mice

S‐Allyl‐L‐Cysteine Sulfoxide Inhibits Tumor Necrosis Factor‐Alpha Induced Monocyte Adhesion and Intercellular Cell Adhesion Molecule‐1 Expression in Human Umbilical Vein Endothelial Cells

Wnt Signaling in Cardiac Disease

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