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Correlation between HDAC4 enhancer DNA methylation and mRNA expression during palatal fusion induced by all-trans retinoic acid.

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Epithelial-mesenchymal transformation of the medial edge epithelium is the most crucial process in embryonic palatal fusion. This study aimed to explore the relationship and potential mechanism between enhancer DNA methylation and mRNA expression of histone deacetylase 4 (HDAC4) during palatal

Processes involved in retinoic acid production of small embryonic palatal shelves and limb defects.

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All-trans-retinoic acid (RA) is teratogenic to the embryonic mouse, producing malformations in many developing systems, including the limb bud and palate. High incidences of limb defects and cleft palate are induced at doses which are not maternally toxic and do not increase resorptions. Exposure to

Involvement of RBP4 in all‑trans retinoic acid induced cleft palate.

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The current study was designed to elucidate the mechanism of retinol binding protein 4 (RBP4) in cleft palate induced by all‑trans retinoic acid (atRA). To establish a cleft palate model in C57BL/6J mice, pregnant mice were administered atRA (100 mg/kg) by gavage at the tenth embryonic stage

Relationship of the fistulas to the rectum and genitourinary tract in mouse fetuses with high anorectal malformations induced by all-trans retinoic acid.

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Since high anorectal malformations with fistulae in human embryos and fetuses of successive developmental stages have not been reported, the embryologic relationship between the rectal fistula (RF) and the genitourinary tract (GUT) in high anorectal agenesis (ARA) remains to be elucidated. This

Retinoic acid-induced stress protein synthesis in the mouse.

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We have previously demonstrated that stress proteins (SPs) are synthesized in tissues in which malformations are later observed following treatment with the developmental toxicant, retinoic acid (RA), on day 11 of gestation (GD 11). These proteins were not synthesized in tissues which did not

[Prophylactic administration of all-trans retinoic acid alleviates inflammation in rats with collagen-induced arthritis].

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OBJECTIVE To investigate the effects of prophylactic administration of all-trans retinoic acid (ATRA) in relieving inflammation in a rat model of collagen-induced arthritis (CIA). METHODS Female Wistar rats (6 to 8 weeks old) were randomly divided into normal control group, solvent control group,

All-trans retinoic acid stimulates gene expression of the cardioprotective natriuretic peptide system and prevents fibrosis and apoptosis in cardiomyocytes of obese ob/ob mice.

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In hypertensive rodents, retinoic acid (RA) prevents adverse cardiac remodelling and improves myocardial infarction outcome, but its role in obesity-related changes of cardiac tissue are unclear. We hypothesized that all-trans RA (ATRA) treatment will improve the cardioprotective

Enhancement of the teratogenicity of all-trans-retinoic acid by maternal restraint stress in mice as a function of treatment timing.

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In CD-1 mice, maternal restraint stress was combined with all-trans-retinoic acid (tRA) given during the restraint period (9:00 a.m. to 9:00 p.m.) to determine in what manner and to what degree teratogenesis might be affected by treatment timing within the stress period and to determine the optimum

Reduction of all-trans-retinoic acid-induced teratogenesis in the rat by glycine administration.

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BACKGROUND Prenatal rat embryo exposure to retinoids induces severe malformations in various organs; the most active and teratogenic metabolite is all-trans-retinoic acid (atRA). The mechanisms of this embryopathy are only partly known. In the present study, the influence of glycine on the

[Induced cleft palat by Retinoic acid through altering the cell proliferation and apoptosis at the key stages of palatal development].

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To investigate the effects of retinoic acid (RA) on the proliferation and apoptosis of mesenchyme and epithelium at the key stages of palatal development, and to determine the embryonic alterations associated with cleft palate. 100 pregnant C57 females (E12) were equally divided into two groups. The

Common differentially expressed proteins were found in mouse cleft palate models induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin and retinoic acid.

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Cleft palate(CP) is a widely studied congenital malformation. However, its etiology and pathogenesis still remain unclear. Proteins are fundamental molecules that participate in every biological process within cells. In this study, we established CP mouse models induced by

Dose-Dependent Antiteratogenic Effects of Folic Acid on All-Trans Retinoic Acid-Induced Cleft Palate in Fetal Mice.

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Although numerous studies have confirmed that consumption of folic acid (FA) during early pregnancy reduces the risk of oral facial clefts in newborn infants, the optimal dose of FA for reducing this risk remains unknown. We evaluated various doses of FA for their ability to reduce the incidence of

All-trans-retinoic acid decreases cell proliferation and increases apoptosis in an animal model of vein bypass grafting.

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BACKGROUND We have previously demonstrated a decrease in intimal hyperplasia in vein bypass grafts from animals treated with all-trans-retinoic acid (atRA). The purpose of this study was to examine the effect of atRA on proliferation and apoptosis rates in healing vein bypass

Induction of maternal toxicity in the rat by dermal application of retinoic acid and its effect on fetal outcome.

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Time-mated Sprague-Dawley rats were administered all-trans-retinoic acid (RA) dermally on gestational days 11 through 14 at three dosage levels (25, 100, and 250 mg/kg body weight). Dams administered ethylenethiourea (ETU) dermally on gestational days 11 to 12 or RA orally on day 12 were used to

Inhibition of growth of established N-methyl-N-nitrosourea-induced mammary cancer in rats by retinoic acid and ovariectomy.

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Retinoids are effective in the prevention of N-methyl-N-nitrosourea-induced mammary carcinoma; retinoids and hormonal therapy exert synergy in cancer prevention. In this study, we examined the effects of the dietary supplementation with all-trans retinoic acid (RA) alone or in combination with

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