Transcription Suppression of Thromboxane Receptor Gene Expression by Retinoids in Vascular Smooth Muscle Cells

Uruno, Akira; Sugawara, Akira; Kudo, Masataka; Sato, Minoru; Sato, Kazunori; Ito, Sadayoshi; Takeuchi, Kazuhisa

doi:10.1291/hypres.26.815

Cited by 15 publications

(13 citation statements)

References 35 publications

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“…It also has several biological activities that promote the synthesis of vasorelaxant molecules (17) and inhibit the action of vasoconstrictor agents (19)(20)(21). In addition, it exhibits antithrombotic and antiatherogenic potential (18,(22)(23)(24)(25)(26)(27)(28)(29)(30)(31).…”

Section: Discussionmentioning

confidence: 99%

“…Retinoids also exhibit putatively beneficial biological actions in the cardiovascular system. They increase NO synthesis, modulate hemostatic properties and inhibit endothelin-1 expression in ECs (17)(18)(19), inhibit actions of angiotensin II and TXA 2 receptor expression in vascular SMCs (20,21), reduce monocyte tissue factor (TF) and TF/factor VIIa-dependent arterial thrombosis (22), and exhibit beneficial actions in cardiovascular disease models (23)(24)(25)(26)(27)(28)(29)(30)(31).…”

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confidence: 99%

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Retinoic acid induces PGI synthase expression in human endothelial cells

Camacho

Rodrı́guez

Salazar

et al. 2008

Journal of Lipid Research

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Retinoic acid (RA) exhibits anti-inflammatory, anti-tumor, and immuno-modulatory actions, and affects angiogenesis and thrombosis. Arachidonic acid (AA) metabolites are involved in all these processes. We explored the effect of RA on AA metabolism in human umbilical vein endothelial cells (HUVECs). 13-cis -RA increased the release of prostaglandin I 2 (PGI 2) , both spontaneous and thrombin-induced, in terms of 6-oxo-PGF 1a analyzed by enzyme-immunoassay. Coincubation with 13-cis-RA and interleukin-1b resulted in a synergic increase in the release of PGI 2 . Consistently, 13-cis -RA increased the ability of HUVECs to inhibit AA-induced platelet aggregation. 13-cis-RA did not induce cyclooxygenase-isoenzyme expression, determined by immunoblotting, or activity, evaluated by analyzing eicosanoids formed from exogenous labeled AA by HPLC. In contrast, RA induced PGI synthase (PGIS) activity and expression in terms of mRNA and protein determined by real-time PCR and Western blotting, respectively. Results from experiments with several species of RA and with retinoic acid receptor (RAR) and retinoid X receptor (RXR) antagonists showed that the effect of RA on PGIS expression was mediated by RAR. Actinomycin D and cycloheximide both inhibited RA-induced PGIS expression. Furthermore, RA increased PGIS transcriptional activity in transient transfection assays, an effect that was prevented by an RAR antagonist. These results reinforce the concept that RA could be beneficial for patients with cardiovascular risk.-Camacho, M., C. Rodríguez, J. Salazar, J. Martínez-González, J. Ribalta, J-R. Escudero, L. Masana, and L. Vila. Retinoic acid induces PGI synthase expression in human endothelial cells.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Retinoic acid induces PGI synthase expression in human endothelial cells

Camacho

Rodrı́guez

Salazar

et al. 2008

Journal of Lipid Research

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“…9cRA has also been reported to inhibit ACTH secretion in dogs with Cushing's disease [15]. Although ATRA is known to bind to RAR, it can intracellularly be isomerized to 9cRA that can bind both to RAR and RXR [1]. Moreover, ATRA is known to activate protein kinase C-δ independent of RAR [4].…”

Section: Roles Of Transcription Factors Tpit and Neurod1 On The Am80-mentioning

confidence: 99%

Retinoic acid receptor-α up-regulates proopiomelanocortin gene expression in AtT20 corticotroph cells

et al. 2014

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“…However, TP receptor gene transcription is suppressed by peroxisome proliferator-activated receptor γ (PPARγ) and retinoids in VSMCs [10, 11]. Growth factors such as platelet-derived growth factor and basic fibroblast growth factor can modify TP receptor expression [12].…”

Section: Introductionmentioning

confidence: 99%

“…In placentas from diabetic pregnancies, TP receptor affinity and vasoconstrictor responses to U46619 are reduced [14]. TP receptor gene transcription is reported to be suppressed by PPARγ and retinoids in VSMCs [10, 11]. Although ovariectomized rats exhibit enhanced vasoconstrictor responses to U46619, oestrogen replacement reduced TP receptor-mediated vasoconstriction [15].…”

Section: Introductionmentioning

confidence: 99%

Transcriptional Down-Regulation of Thromboxane A<sub>2</sub> Receptor Expression via Activation of MAPK ERK1/2, p38/NF-κB Pathways

Zhang¹,

Zhang

Edvinsson

et al. 2008

J Vasc Res

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Background: We have developed an in vitro model by organ culture of rat mesenteric arteries to imitate vascular smooth muscle cell (VSMC) receptor changes in cardiovascular disease. By using this model, alteration of VSMC thromboxane A₂ (TP) receptors was studied. Methods and Results:After organ culture of the arteries, VSMC TP receptors were studied by using myography, real-time PCR and immunohistochemistry. We observed that organ culture for 24 and 48 h resulted in depressed TP receptor-mediated contraction in the VSMC, in parallel with decreased TP receptor mRNA and protein expressions. Phosphorylation of extracellular signal-regulated kinase 1 and 2 (ERK1/2), p38 and nuclear factor-κB (NF-κB) was seen by Western blot within 1–3 h after organ culture. Inhibition of ERK1/2, p38 or NF-κB reversed depressed contraction as well as decreased receptor mRNA expression. Actinomycin D abolished decreased TP receptor-mediated contraction, while inhibition of translation, cyclooxygenase or nitric oxide synthase had no effect. TP receptor mRNA stability was unchanged during organ culture. Conclusions:The present study has demonstrated for the first time that organ culture of rat mesenteric arteries down-regulates VSMC TP receptor expression through activation of ERK1/2 and p38/NF-κB signal pathways.

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Transcription Suppression of Thromboxane Receptor Gene Expression by Retinoids in Vascular Smooth Muscle Cells

Cited by 15 publications

References 35 publications

Retinoic acid induces PGI synthase expression in human endothelial cells

Retinoic acid induces PGI synthase expression in human endothelial cells

Retinoic acid receptor-α up-regulates proopiomelanocortin gene expression in AtT20 corticotroph cells

Transcriptional Down-Regulation of Thromboxane A<sub>2</sub> Receptor Expression via Activation of MAPK ERK1/2, p38/NF-κB Pathways

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