Sulforaphane suppresses vascular adhesion molecule-1 expression in TNF-α-stimulated mouse vascular smooth muscle cells: Involvement of the MAPK, NF-κB and AP-1 signaling pathways

Kim, Jiyun; Park, Hye-Jin; Um, Sung Hee; Sohn, Eun‐Hwa; Kim, Byung-Oh; Moon, Eun‐Yi; Rhee, Dong‐Kwon; Pyo, Suhkneung

doi:10.1016/j.vph.2011.11.007

Cited by 57 publications

(54 citation statements)

References 51 publications

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“…Our results demonstrate that treatment with EGF induced upregulation of VCAM-1 expression in GBM cells in a NF-B-dependent manner, which is in line with previous reports demonstrating that the promoter region of the VCAM-1 gene contains NF-B-binding sites (30,42) and that activation of NF-B stimulates VCAM-1 expression (38,43,44). In addition, via direct interaction with tumor cells, macrophages significantly induce activation of STAT-3 (signal transducer and activator of transcription-3) in the tumor cells (45).…”

Section: Discussionsupporting

confidence: 93%

Epidermal Growth Factor (EGF)-enhanced Vascular Cell Adhesion Molecule-1 (VCAM-1) Expression Promotes Macrophage and Glioblastoma Cell Interaction and Tumor Cell Invasion

Zheng¹,

Yang²,

Aldape³

et al. 2013

Journal of Biological Chemistry

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Background:The mechanism underlying EGF receptor (EGFR) activation-promoted glioblastoma (GBM) cell invasion remains elusive. Results: EGFR activation resulted in PKC⑀-and NF-B-dependent VCAM-1 up-regulation, which subsequently promoted the interaction between macrophages and GBM cells, as well as GBM cell invasion. Conclusion: EGF-induced VCAM-1 up-regulation plays an instrumental role in EGFR activation-promoted macrophagetumor cell interaction and tumor cell invasion. Significance: VCAM-1 expression is a potential target for GBM therapy.

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Section: Discussionsupporting

confidence: 93%

Epidermal Growth Factor (EGF)-enhanced Vascular Cell Adhesion Molecule-1 (VCAM-1) Expression Promotes Macrophage and Glioblastoma Cell Interaction and Tumor Cell Invasion

Zheng¹,

Yang²,

Aldape³

et al. 2013

Journal of Biological Chemistry

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“…Supporting its anti-inflammatory and cardiovascular protective properties, SFN can inhibit TNF-a-induced adhesion molecule expression through the inhibition of MAPK, NF-jB, and AP-1 signaling pathways and intracellular ROS production. 50 Furthermore, SFN inhibits neointima formation using targeting adhesion molecules through the suppression of NFjB/GATA6, and regulates migration and proliferation in VSMCs. 51 SFN also induces multiple anti-oxidant enzymes through activation of Nrf2 transcription factor 52 and inhibits EL expression through inhibition of NF-jB, which may have a beneficial effect on HDL cholesterol levels.…”

Section: Discussionmentioning

confidence: 99%

Sulforaphane Inhibits TNF-α-Induced Adhesion Molecule Expression Through the Rho A/ROCK/NF-κB Signaling Pathway

Hung

Huang

Wang

et al. 2014

Journal of Medicinal Food

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Endothelial dysfunction is an early indicator of cardiovascular diseases. Increased stimulation of tumor necrosis factor-a (TNF-a) triggers the inflammatory mediator secretion of endothelial cells, leading to atherosclerotic risk. In this study, we investigated whether sulforaphane (SFN) affected the expression of intracellular adhesion molecule-1 (ICAM-1) in TNF-a-induced ECV 304 endothelial cells. Our data showed that SFN attenuated TNF-a-induced expression of ICAM-1 in ECV 304 cells. Pretreatment of ECV 304 cells with SFN inhibited dose-dependently the secretion of proinflammatory cytokines, such as interleukin (IL)-1b, IL-6, and IL-8. SFN inhibited TNF-a-induced nuclear factor-jB (NF-jB) DNA binding activity. Furthermore, SFN decreased TNF-a-mediated phosphorylation of IjB kinase (IKK) and IjBa, Rho A, ROCK, ERK1/ 2, and plasminogen activator inhibitor-1 (PAI-1) levels. Collectively, SFN inhibited the NF-jB DNA binding activity and downregulated the TNF-a-mediated induction of ICAM-1 in endothelial cells by inhibiting the Rho A/ROCK/NF-jB signaling pathway, suggesting the beneficial effects of SFN on suppression of inflammation within the atherosclerotic lesion.

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“…In human atherosclerotic plaques expression of VCAM-1 is increased in smooth muscle cells. 27) it reported that the effect of statins decreasing the number of macrophages is associated with decreased VCAM-1 expression, higher VSMC content in the plaque. [28][29][30] Our data show that the effects of 3,4-DHAP are similar to simvastatin, decreasing the expressions of VCAM-1 mRNA and protein and the number of macrophage, and increasing VSMCs in rabbit aortic plaques.…”

Section: 4-dhap Attenuates Aortic Plaque Vulnerability By Decreasinmentioning

confidence: 98%

Effects of 3,4-Dihydroxyacetophenone on the Hypercholesterolemia-Induced Atherosclerotic Rabbits

Zhang

Liu

Wang

et al. 2013

Biological & Pharmaceutical Bulletin

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3,4-Dihydroxyacetophenone (3,4-DHAP) is one herbal extract from bald Mao-dong-qing leaves. We reported that 3,4-DHAP had anti-inflammatory function by decreasing tumor necrosis factor-α (TNF-α) secretion in macrophages. The aim of the study was to examine the effects of 3,4-DHAP on plasma and liver lipids, plasma alanine aminotranferase (ALT) and TNF-α level, vascular cell adhesion molecule-1 (VCAM-1) expression, plaque vulnerability and vascular inflammation in hypercholesterolemia-induced atherosclerotic rabbits. Male New Zealand white rabbits were randomized into negative control, positive control, 3,4-DHAP and simvastatin groups. From weeks 2 to 12, the rabbits were treated with 3,4-DHAP or simvastatin. At weeks 12, all the animals were sacrificed. Plasma lipids and ALT were measured using the enzymatic endpoint method. Plasma TNF-α was measured using enzyme-linked immuno sorbent assay (ELISA). Liver lipids concentrations were estimated using commercial kits. The expression of VCAM-1 was measured using reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. Histological analysis was used to evaluate the pathologic changes of rabbit aortas. The results showed that 3,4-DHAP markedly lowered plasma and liver lipids, lowered plasma ALT and TNF-α levels compared with the positive control group. VCAM-1 mRNA and protein were markedly inhibited by 3,4-DHAP. Decreased aortic plaque instability was evident in 3,4-DHAP-treated rabbits, as demonstrated by a thickened elastic layer, increased vascular smooth muscle cells (VSMCs) accumulation in the plaques, less neointima hyperplasia and macrophages recruitment. 3,4-DHAP may attenuate the progression of atherosclerotic lesions and stabilize plaques by lowering plasma lipids, the number of macrophages and the expression of VCAM-1, while increasing the number of VSMCs in the atherosclerotic plaques. Key words 3,4-dihydroxyacetophenone; vascular cell adhesion molecule-1; atherosclerosisAtherosclerosis is an inflammatory disease.1) Atherosclerosis associated with the rupture of vulnerable plaque is the main cause of cardiovascular events. The characteristics of vulnerable plaque include a large lipid core, thin fibrous cap, inflammation and immune cell activation.2) Growing evidence shows that macrophages play a pivotal role in all stages of atherosclerosis. Vascular cell adhesion molecule-1 (VCAM-1) can strength the adhesion of leukocytes to vascular wall, promote leukocytes entering intima, transforming into macrophages. 3)Evidence is accumulating that low-density lipoprotein cholesterol (LDL-C) is the principal risk factor for atherosclerosis, and it is identified as the primary target for cholesterol-lowering therapy.4) Tumor necrosis factor-α (TNF-α) is one of the most important mediators of inflammation and may mediate endothelial dysfunction. 5,6)3,4-Dihydroxyacetophenone (3,4-DHAP) is extracted from herb; clinical experiments and pharmacological studies of it have been on for many years in coronary heart disease, pregnancy-induced hypertension synd...

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Sulforaphane suppresses vascular adhesion molecule-1 expression in TNF-α-stimulated mouse vascular smooth muscle cells: Involvement of the MAPK, NF-κB and AP-1 signaling pathways

Cited by 57 publications

References 51 publications

Epidermal Growth Factor (EGF)-enhanced Vascular Cell Adhesion Molecule-1 (VCAM-1) Expression Promotes Macrophage and Glioblastoma Cell Interaction and Tumor Cell Invasion

Epidermal Growth Factor (EGF)-enhanced Vascular Cell Adhesion Molecule-1 (VCAM-1) Expression Promotes Macrophage and Glioblastoma Cell Interaction and Tumor Cell Invasion

Sulforaphane Inhibits TNF-α-Induced Adhesion Molecule Expression Through the Rho A/ROCK/NF-κB Signaling Pathway

Effects of 3,4-Dihydroxyacetophenone on the Hypercholesterolemia-Induced Atherosclerotic Rabbits

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