Up-regulation of thromboxane A2 receptor expression by lipid soluble smoking particles through post-transcriptional mechanisms

Zhang, Wei; Zhang, Yaping; Edvinsson, Lars; Xu, Cang‐Bao

doi:10.1016/j.atherosclerosis.2007.06.031

Cited by 24 publications

(15 citation statements)

References 45 publications

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“…In previous experiments, we found that the addition of 1 μl DMSO to the 1 ml DMEM did not modify the upregulation of receptors. The PKC pathway inhibitor was staurosporine (0.1 μM) [28], and the inhibitors selected to target different kinases leading to ERK1/2 activation were U0126 (10 μM) [13] and SB386023 (10 μM) [29]. U0126 is an inhibitor of the MAP kinase/ERK kinase (MEK) 1/2, the MAPKK of ERK1/2, while SB386023 inhibits raf, the MAPKKK of ERK1/2.…”

Section: Preparation Of Coronary Arterial Segments and Organ Culturementioning

confidence: 99%

“…The ET B receptor is the principal receptor involved in the progression of coronary vascular diseases [5,7]. We previously developed an organ culture model that can mimic the upregulation of ETB receptors in cardiovascular disease [11][12][13][14][15]. Using this model, we demonstrated that the upregulation of ET B receptors induced by organ culture of arteries is via activation of mitogen-activated protein kinase (MAPK) and the downstream nuclear factor-kappaB (NF-κB) intracellular signal transduction pathways [14,15].…”

Section: Introductionmentioning

confidence: 99%

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Minimally modified LDL upregulates endothelin type B receptors in rat coronary artery via ERK1/2 MAPK and NF-κB pathways

Cao

Yuan

et al. 2012

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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Minimally modified low density lipoprotein (mmLDL) is a well-known risk factor for coronary artery disease. Upregulation of vascular endothelin type B (ET B ) receptors on the vascular smooth muscle cells is predicted to be the molecular mechanism that leads to cardiovascular pathogenesis. The objective of the present study was to examine the hypothesis that mmLDL upregulates ET B receptors in rat coronary artery. The contractile responses to sarafotoxin 6c (ET B receptor agonist) were studied using a sensitive myograph. ETB receptor mRNA and protein expression was determined using real-time PCR and Western blot analysis.The results showed that organ culture increased the contractile responses induced by sarafotoxin 6c and the levels of ET B receptor mRNA and protein. This increase was further enhanced by the addition of mmLDL (10 μg/mL). Specific ERK1/2 inhibitors (SB386023 and U0126) and an NF-κB inhibitor (wedelolactone) attenuated the mmLDL-increased ET B receptor-mediated contraction and ET B receptor mRNA and protein levels. Wedelolactone significantly attenuated the mmLDL-decreased IκBα protein expression. Consistent with this result, IκBα protein expression was significantly decreased by culture withmmLDL compared to the level of expression in the organ culture group. However, the JNK inhibitor, SP600125 or p38 pathway inhibitor, SB203580 did not inhibit mmLDL-enhanced effects. The PKC inhibitor, staurosporine attenuated only culture-alone-increased effects. In conclusion, mmLDL upregulates the ETB receptors in rat coronary arterial smooth muscle cells, mainly via activation of the ERK1/2 MAPK and the downstream transcriptional factor NF-κB.

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Section: Preparation Of Coronary Arterial Segments and Organ Culturementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Minimally modified LDL upregulates endothelin type B receptors in rat coronary artery via ERK1/2 MAPK and NF-κB pathways

Cao

Yuan

et al. 2012

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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“…Sections were cut at 10-µm thickness in a cryostat and mounted on SuperFrost Plus slides (Menzel-Gläser, Braunschweig, Germany). Immunohistochemistry was carried out using standard protocols Zhang et al, 2008).…”

Section: Immunohistochemistry With Confocal Microscopymentioning

confidence: 99%

Apolipoprotein B of low-density lipoprotein impairs nitric oxide-mediated endothelium-dependent relaxation in rat mesenteric arteries

Zhang

Edvinsson

et al. 2014

European Journal of Pharmacology

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“…16 Recently, heptane-soluble, DMSO-soluble and water-soluble cigarette smoke particles and their effects on G-protein coupled receptor expression were investigated (unpublished data). These results show that it is the lipidsoluble cigarette smoke particles, but not water soluble or nicotine per se, increase the gene expression for G-protein coupled receptors in the arterial smooth muscle cells 16,22 as well as induce damage of the endothelium and its functions. 31 AT 1 receptors mediate strong contraction of arteries and involve in vascular infl ammation.…”

Section: Vikman Et Almentioning

confidence: 80%

“…We have studied the time course of DSP and the DSP dose-dependent effects previously 8,16,22 The results show that DSP dose-dependently triggers the arterial smooth muscle cells and induces effects starting at concentration 0.1 μl/ml and reaching its maximal effect at 0.2 μl/ml and declining at 0.4 μl/ml. The time course study shows that DSP induces activation (phosphorylation) of p38 within 3 h and further increasing the activation during 24 h. This is associated with upregulation of ET B receptor protein expression at 6 h, assessed by Western blot in the arterial smooth muscle cells.…”

Section: Vikman Et Almentioning

confidence: 99%

Lipid-soluble cigarette smoking particles induce expression of inflammatory and extracellular-matrix-related genes in rat cerebral arteries

Vikman¹,

Xu²,

Edvinsson³

2009

VHRM

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Aims: Cigarette smoking is one of the strongest risk factors for stroke. However, the underlying molecular mechanisms that smoke leads to the pathogenesis of stroke are incompletely understood. Methods: Dimethyl sulfoxide (DMSO)-soluble (lipid-soluble) cigarette smoking particles (DSP) were extracted from cigarette smoke (0.8 mg nicotine per cigarette; Marlboro ® ). Rat cerebral arteries were isolated and organ cultured in the presence of DSP (0.2 μl/ml, equivalent to the plasma level in smokers) for 24 h. The expression of matrix metalloproteinase 9 and 13 (MMP9 and MMP13), angiotensin receptor 1 and 2 (AT 1 and AT 2 ), interleukin 6 and inducible nitric oxide synthase (iNOS) were investigated at mRNA level by real-time PCR and/or at protein level by immunohistochemistry. In addition, the activity of three mitogen-activated protein kinases (p38, ERK 1/2 and SAPK/JNK) and their downstream transcription factors (ATF-2, Elk-1 and c-Jun) were examined. Results:We observed that compared with control (DMSO-treated cerebral arteries), the cerebral arteries treated by DSP exhibited enhanced expression of MMP13 and AT 1 receptors, but not of AT 2 receptors, at both mRNA and protein levels, suggesting that a transcriptional mechanism is most likely involved in the DSP effects. This is further supported by the fi ndings that DSP induced phosphorylation of p38 mitogen-activated protein kinases infl ammatory signal protein in parallel with activation of its downstream transcription factor ATF-2 and Elk-1. However, ERK 1/2 and SAPK/JNK activities were markedly expressed in the control (organ culture per se with DMSO), and DSP failed to further enhance the activation of ERK 1/2 and SAPK/JNK in the cerebral arteries. Conclusions: DSP induces cerebral vessel infl ammation with activation of p38 MAPK infl ammatory signal and the downstream transcriptional factors (ATF-2 and Elk-1) in parallel with enhanced extracellular-matrix-related gene transcription and increased AT 1 receptor expression in the cerebral arteries, which are key events in stroke pathogenesis.

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Up-regulation of thromboxane A2 receptor expression by lipid soluble smoking particles through post-transcriptional mechanisms

Cited by 24 publications

References 45 publications

Minimally modified LDL upregulates endothelin type B receptors in rat coronary artery via ERK1/2 MAPK and NF-κB pathways

Minimally modified LDL upregulates endothelin type B receptors in rat coronary artery via ERK1/2 MAPK and NF-κB pathways

Apolipoprotein B of low-density lipoprotein impairs nitric oxide-mediated endothelium-dependent relaxation in rat mesenteric arteries

Lipid-soluble cigarette smoking particles induce expression of inflammatory and extracellular-matrix-related genes in rat cerebral arteries

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