Retinoic acid suppresses endothelin-1 gene expression at the transcription level in endothelial cells

Yokota, Jinko; Kawana, Masatoshi; Hidai, Chiaki; Aoka, Yoshikazu; Ichikawa, Kenichiro; Iguchi, Nobuo; Okada, Minoru; Kasanuki, Hiroshi

doi:10.1016/s0021-9150(01)00530-5

Cited by 23 publications

(29 citation statements)

References 22 publications

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“…Typically, targets are upregulated by RA not down-regulated as described here for Tbx1, although down-regulation of endothelin-1, a Tbx1 target gene, (Piotrowski et al, 2003), has been described in endothelial cells 8 hr after the addition of RA (Yokota et al, 2001). As some of the repression we observed was dependent upon de novo protein synthesis, it is possible that an intermediary transcriptional repressor is involved.…”

Section: Discussionmentioning

confidence: 53%

Retinoic acid down‐regulates Tbx1 expression in vivo and in vitro

Roberts¹,

Ivins²,

James³

et al. 2005

Developmental Dynamics

105

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Both Tbx1 and retinoic acid (RA) are key players in embryonic pharyngeal development; loss of Tbx1 produces DiGeorge syndrome-like phenotypes in mouse models as does disruption of retinoic acid homeostasis. We have demonstrated that perturbation of retinoic acid levels in the avian embryo produces altered Tbx1 expression. In vitamin A-deficient quails, which lack endogenous retinoic acid, Tbx1 expression patterns were disrupted early in development and expression was subsequently lost in all tissues. "Gain-of-function" experiments where RA-soaked beads were grafted into the pharyngeal region produced localized down-regulation of Tbx1 expression. In these embryos, analysis of Shh and Foxa2, upstream control factors for Tbx1, suggested that the effect of RA was independent of this regulatory pathway. Real-time polymerase chain reaction analysis of retinoic acid-treated P19 cells showed a dosedependent repression of Tbx1 by retinoic acid. Repression of Tbx1 transcript levels was first evident after 8 -12 hr in culture in the presence of retinoic acid, and to achieve the highest levels of repression, de novo protein synthesis was required. Developmental Dynamics 232:928 -938, 2005.

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Section: Discussionmentioning

confidence: 53%

Retinoic acid down‐regulates Tbx1 expression in vivo and in vitro

Roberts¹,

Ivins²,

James³

et al. 2005

Developmental Dynamics

105

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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).…”

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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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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“…Les acides rétinoïques inhibent la croissance cellulaire, et ont donc une action anti-athérogène potentielle dans les vaisseaux. Les acides rétinoïques répriment égale-ment l'expression de l'ARNm codant pour la PPET-1 et l'activité transcriptionnelle de son promoteur [14]. Ces résultats suggèrent que les rétinoïdes pourraient être des modulateurs de la fonction endothéliale.…”

Section: Modulation Du Système Endothélineunclassified

À quoi sert le système endothéline ?

Pinet

2004

Med Sci (Paris)

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Retinoic acid suppresses endothelin-1 gene expression at the transcription level in endothelial cells

Cited by 23 publications

References 22 publications

Retinoic acid down‐regulates Tbx1 expression in vivo and in vitro

Retinoic acid down‐regulates Tbx1 expression in vivo and in vitro

Retinoic acid induces PGI synthase expression in human endothelial cells

À quoi sert le système endothéline ?

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