Emodin suppresses lipopolysaccharide‐induced pro‐inflammatory responses and NF‐κB activation by disrupting lipid rafts in CD14‐negative endothelial cells

Meng, Guoquan; Liu, Yiyao; Lou, Changchun; Yang, Hong

doi:10.1111/j.1476-5381.2010.00993.x

Cited by 85 publications

(59 citation statements)

References 38 publications

(39 reference statements)

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“…Lipid rafts have also been reported to be essential for NF-kB activation induced by a diverse set of stimuli, such as interleukin (IL)-1b, CD40L, and lipopolysaccharides (LPS; refs. 8,9,12). Collectively, these findings indicate that lipid rafts play important roles in the activation of proximal NF-kB signaling.…”

Section: Introductionmentioning

confidence: 70%

Downregulation of miR-138 Sustains NF-κB Activation and Promotes Lipid Raft Formation in Esophageal Squamous Cell Carcinoma

Gong

Song

Lin

et al. 2013

Clinical Cancer Research

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Purpose: Constitutive activation of NF-kB signaling plays vital roles in esophageal squamous cell carcinoma (ESCC) progression. The aim of this study was to evaluate the effect of miR-138 on NF-kB activation and ESCC progression.Experimental Design: Expression of miR-138 in ESCC cell lines, ESCC tissues, and 205 archived ESSC specimens was determined using real-time PCR analysis. Anchorage-independent growth, chicken chorioallantoic membrane, Transwell matrix invasion and Annexin V-binding assays, and a xenograft tumor model were used to determine the role of miR-138 in ESCC progression. The effect of miR-138 on NF-kB activation was investigated using IKK in vitro kinase, electrophoretic mobility shift, lipid raft isolation, and luciferase reporter assays.Results: miR-138 was downregulated and inversely correlated with tumor progression and patient survival in ESCCs. Downregulation of miR-138 enhanced, whereas upregulation of miR-138 reduced, the aggressive phenotype of ESCC cells both in vitro and in vivo. Silencing miR-138 promoted K63-linked polyubiquitination of the NF-kB signaling intermediaries TRAF2 and RIP1 and sustained NF-kB activation. Furthermore, downregulation of miR-138 induced lipid raft formation via upregulating multiple components of lipid rafts, including FLOT1, FLOT2, and caveolin-1. Importantly, the in vitro analysis was consistent with a significant inverse correlation between miR-138 expression and NF-kB hyperactivation in a cohort of human ESCC specimens.Conclusion: Our results show that miR-138 functions as a tumor-suppressive miRNA and that downregulation of miR-138 contributes to constitutive NF-kB activation and ESCC progression.

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Section: Introductionmentioning

confidence: 70%

Downregulation of miR-138 Sustains NF-κB Activation and Promotes Lipid Raft Formation in Esophageal Squamous Cell Carcinoma

Gong

Song

Lin

et al. 2013

Clinical Cancer Research

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“…Inflamed endothelial cells express and release a range of proinflammatory cytokines, chemokines, and adhesion molecules, which are vital to evoke innate immune response and endothelial dysfunction (Meng et al 2010;Zeng et al 2005).…”

Section: Introductionmentioning

confidence: 99%

Sodium tanshinone IIA sulfonate prevents lipopolysaccharide-induced inflammation via suppressing nuclear factor-κB signaling pathway in human umbilical vein endothelial cells

Cheng

Chen

et al. 2018

Can. J. Physiol. Pharmacol.

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“…The cultured HUVEC-CS were stimulated with 1 µg/mL lipopolysaccharide for five hours to induce inflammation. 19 …”

Section: Cell Culturementioning

confidence: 99%

VCAM-1-targeted core/shell nanoparticles for selective adhesion and delivery to endothelial cells with lipopolysaccharide-induced inflammation under shear flow and cellular magnetic resonance imaging in vitro

Yang¹,

Zhao²,

Liu³

et al. 2013

IJN

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Multifunctional nanomaterials with unique magnetic and luminescent properties have broad potential in biological applications. Because of the overexpression of vascular cell adhesion molecule-1 (VCAM-1) receptors in inflammatory endothelial cells as compared with normal endothelial cells, an anti-VCAM-1 monoclonal antibody can be used as a targeting ligand. Herein we describe the development of multifunctional core-shell Fe 3 O 4 @SiO 2 nanoparticles with the ability to target inflammatory endothelial cells via VCAM-1, magnetism, and fluorescence imaging, with efficient magnetic resonance imaging contrast characteristics. Superparamagnetic iron oxide and fluorescein isothiocyanate (FITC) were loaded successfully inside the nanoparticle core and the silica shell, respectively, creating VCAM-1-targeted Fe 3 O 4 @ SiO 2 (FITC) nanoparticles that were characterized by scanning electron microscopy, transmission electron microscopy, fluorescence spectrometry, zeta potential assay, and fluorescence microscopy. The VCAM-1-targeted Fe 3 O 4 @SiO 2 (FITC) nanoparticles typically had a diameter of 355 ± 37 nm, showed superparamagnetic behavior at room temperature, and cumulative and targeted adhesion to an inflammatory subline of human umbilical vein endothelial cells (HUVEC-CS) activated by lipopolysaccharide. Further, our data show that adhesion of VCAM-1-targeted Fe 3 O 4 @SiO 2 (FITC) nanoparticles to inflammatory HUVEC-CS depended on both shear stress and duration of exposure to stress. Analysis of internalization into HUVEC-CS showed that the efficiency of delivery of VCAM-1-targeted Fe 3 O 4 @SiO 2 (FITC) nanoparticles was also significantly greater than that of nontargeted Fe 3 O 4 @SiO 2 (FITC)-NH 2 nanoparticles. Magnetic resonance images showed that the superparamagnetic iron oxide cores of the VCAM-1-targeted Fe 3 O 4 @SiO 2 (FITC) nanoparticles could also act as a contrast agent for magnetic resonance imaging. Taken together, the cumulative adhesion and uptake potential of these VCAM-1-targeted Fe 3 O 4 @SiO 2 (FITC) nanoparticles targeted to inflammatory endothelial cells could be used in the transfer of therapeutic drugs/genes into these cells or for diagnosis of vascular disease at the molecular and cellular levels in the future.

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Emodin suppresses lipopolysaccharide‐induced pro‐inflammatory responses and NF‐κB activation by disrupting lipid rafts in CD14‐negative endothelial cells

Cited by 85 publications

References 38 publications

Downregulation of miR-138 Sustains NF-κB Activation and Promotes Lipid Raft Formation in Esophageal Squamous Cell Carcinoma

Downregulation of miR-138 Sustains NF-κB Activation and Promotes Lipid Raft Formation in Esophageal Squamous Cell Carcinoma

Sodium tanshinone IIA sulfonate prevents lipopolysaccharide-induced inflammation via suppressing nuclear factor-κB signaling pathway in human umbilical vein endothelial cells

VCAM-1-targeted core/shell nanoparticles for selective adhesion and delivery to endothelial cells with lipopolysaccharide-induced inflammation under shear flow and cellular magnetic resonance imaging in vitro

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