Mitogen-activated protein kinase (MAPK)

Cuschieri, Joseph; Maier, Ronald V.

doi:10.1097/01.ccm.0000191714.39495.a6

Cited by 79 publications

(82 citation statements)

References 17 publications

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“…Data have shown that the activation of MAPK is closely related to the ROS activity and local oxidative stress. 26) Through changes in MAPK activation, Rb1 treatment may lead to downstream changes in VCAM-1 mRNA and protein expression as well as cell adhesion.…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rb1 Inhibits Tumor Necrosis Factor-.ALPHA.-Induced Vascular Cell Adhesion Molecule-1 Expression in Human Endothelial Cells

Chai

Wang

Huang

et al. 2008

Biological & Pharmaceutical Bulletin

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Section: Discussionmentioning

confidence: 99%

Ginsenoside Rb1 Inhibits Tumor Necrosis Factor-.ALPHA.-Induced Vascular Cell Adhesion Molecule-1 Expression in Human Endothelial Cells

Chai

Wang

Huang

et al. 2008

Biological & Pharmaceutical Bulletin

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“…The MAPK family is involved in inflammatory factormediated signaling (Cuschieri and Maier, 2005). To understand the mechanism(s) underlying the action of ACSO in TNF-a-mediated HUVEC activation, we examined the impact of ACSO treatment on the phosphorylation of ERKl/2, p38 and JNK in HUVECs following treatment with TNF-a in vitro.…”

Section: Acso Inhibits Tnf-a-induced Icam-1 Expressionmentioning

confidence: 99%

“…Luminex has been recently used for the evaluation of MAPKs and NF-jB phosphorylation (Cuschieri and Maier, 2005). The impact of ACSO treatment on TNF-astimulated phosphorylation of MAPK signaling events and IjB in HUVEC cells were analyzed by Bio-Plex immunoassay using the Bio-Plex Cell Lysis Kit, according to manufacturers' instructions with minor modification (Eyad et al, 2004).…”

Section: Bio-plex Luminex Immunoassaymentioning

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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“…One possible explanation is ERK, JNK and p38 pathways crosstalked each other and this cooperation might be critical for ANX-induced Elk-1 transactivation. This view is supported by the notion that MAPK pathways often shares upstream and downstream kinases and transcription factors that interact and integrate among different MAPK cascades (Cuschieri and Maier, 2005). Further study will be required to determine the detailed mechanisms underlying the regulation of ERK, JNK and p38 MAPK pathways by ANX.…”

Section: Discussionmentioning

confidence: 68%

The translation inhibitor anisomycin induces Elk-1-mediated transcriptional activation of egr-1 through multiple mitogen-activated protein kinase pathways

Shin¹,

Lee²,

Min³

et al. 2006

Exp Mol Med

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The early growth response-1 gene (egr-1) encodes a zinc-finger transcription factor Egr-1 and is rapidly inducible by a variety of extracellular stimuli. Anisomycin (ANX), a protein synthesis inhibitor, stimulates mitogen-activated protein kinase (MAPK) pathways and thereby causes a rapid induction of immediate-early response genes. We found that anisomycin treatment of U87MG glioma cells resulted in a marked, time-dependent increase in levels of Egr-1 protein. The results of Northern blot analysis and reporter gene assay of egr-1 gene promoter (P egr-1 ) activity indicate that the ANXinduced increase in Egr-1 occurs at the transcriptional level. Deletion of the serum response element (SRE) in the 5'-flanking region of egr-1 gene abolished ANX-induced Pegr-1 activity. ANX induced the phosphorylation of the ERK1/2, JNK, and p38 MAPKs in a time-dependent manner and also induced transactivation of Gal4-Elk-1, suggesting that Elk-1 is involved in SRE-mediated egr-1 transcription. Transient transfection of dominant-negative constructs of MAPK pathways blocked ANX-induced Pegr-1 activity. Furthermore, pretreatment with specific MAPK pathway inhibitors, including the MEK inhibitor U0126, the JNK inhibitor SP600125, and the p38 kinase inhibitor SB202190, completely inhibited ANX-inducible expression of Egr-1. Taken together, these results suggest that all three MAPK pathways play a crucial role in ANX-induced transcriptional activation of P egr-1 through SRE-mediated transactivation of Elk-1.

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Mitogen-activated protein kinase (MAPK)

Cited by 79 publications

References 17 publications

Ginsenoside Rb1 Inhibits Tumor Necrosis Factor-.ALPHA.-Induced Vascular Cell Adhesion Molecule-1 Expression in Human Endothelial Cells

Ginsenoside Rb1 Inhibits Tumor Necrosis Factor-.ALPHA.-Induced Vascular Cell Adhesion Molecule-1 Expression in Human Endothelial Cells

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

The translation inhibitor anisomycin induces Elk-1-mediated transcriptional activation of egr-1 through multiple mitogen-activated protein kinase pathways

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