scholarly journals Inhibition of periderm removal in all-trans retinoic acid-induced cleft palate in mice

2017 ◽  
Vol 14 (4) ◽  
pp. 3393-3398 ◽  
Author(s):  
Ya-Dong Zhang ◽  
Shi-Yi Dong ◽  
Hong-Zhang Huang
Keyword(s):  
Retinoic Acid ◽  
Cleft Palate ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid

EFFECT OF FETAL EXPOSURE OF ALL-TRANS RETINOIC ACID ON DNA METHYLATION IN MOUSE FETUSES WITH CLEFT PALATE

2007 ◽  
Vol 77 (Suppl_1) ◽  
pp. 162-162
Author(s):  
Yoshiharu Matsuno ◽  
Motone Kuriyama ◽  
Hideki Fukata ◽  
Koji Sato ◽  
Chisato Mori
Keyword(s):  
Dna Methylation ◽  
Retinoic Acid ◽  
Cleft Palate ◽  
Fetal Exposure ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Mouse Fetuses

LncRNA H19-mediated mouse cleft palate induced by all-trans retinoic acid

2016 ◽  
Vol 36 (4) ◽  
pp. 395-401 ◽  
Author(s):  
L Gao ◽  
Y Liu ◽  
Y Wen ◽  
W Wu
Keyword(s):  
Retinoic Acid ◽  
Cleft Palate ◽  
Target Gene ◽  
Functional Roles ◽  
New Class ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Age Related ◽  
And Control

Long noncoding RNAs (lncRNAs) are the new class of transcripts and pervasively transcribed in the genome, which have been found to play important functional roles in many tissues and organs. LncRNAs can interact with target gene to exert their functions. However, the function and mechanism of lncRNA in cleft palate (CP) development remain elusive. Here, we investigated the role of lncRNA H19 and its target gene insulin-like growth factor 2 (IGF2) in CP of mice. All-trans retinoic acid (atRA) is a well-known teratogenic effecter of CP. After establishment of the CP mouse model using atRA in vivo, we found that the rate of CP in mice was 100%. The tail lengths of fetuses in atRA-treated mice were shorter than those of control mice from embryonic day (E)12 to E17. The expression of lncRNA H19 and IGF2 were embryo age-related differences between atRNA-treated and control mice. In addition, the the relationship between lncRNA H19 and IGF2 were negative correlation in the critical period of developmental palate. These findings suggest that lncRNA H19 mediate atRA-induced CP in mice.

scholarly journals All-trans Retinoic Acid Regulates miR-106a-5p Inhibition of Autophagic in Developing Cleft Palates

2020 ◽  
Author(s):  
Lungang Shi ◽  
Yan Liang ◽  
Lijing Yang ◽  
Binchen Li ◽  
Binna Zhang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Retinoic Acid ◽  
Cleft Palate ◽  
Osteogenic Differentiation ◽  
Signaling Pathway ◽  
Differentiation Potential ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Pten Mrna

AbstractBackgroundAll-trans retinoic acid (atRA) results in cleft palate, but the cellular and molecular mechanisms underlying the teratogenic effects on palatal development have not been fully elucidated. Autophagy interruption has been reported to seriously affect embryonic-cell differentiation and development. This study aimed to verify whether atRA-induced cleft palate occurs because atRA blocks autophagy and stemness of embryonic palatal mesenchyme (MEPM) cells, which are maintained via the phosphatase and tensin homolog (PTEN)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) autophagic signaling pathway, and inhibits osteogenic-differentiation potential of MEPM cells, which could lead to the development of cleft palate.MethodsTo assess the stemness and pluripotency of MEPM cells, we analyzed their surfacemarkers using immunofluorescence (IF) and flow cytometry (FCM). Differentiation potentials, such as osteogenic, adipogenic, and chondrogenic differentiation, were induced. We also investigated the role of the PTEN/Akt/mTOR autophagic signaling pathway, which maintains the stemness and pluripotency of MEPM cells. Using transmission electron microscopy (TEM), Western blot analysis, quantitative reverse transcriptase polymerase chain reaction (RT-qPCR), messenger ribonucleic acid (mRNA) microarray, dual-luciferase reporter system, and exosomes, we found that atRA blocks autophagy and osteogenic differentiation of MEPM cells through micro-ribonucleic acid (miR)-106a-5p by targeting the PTEN/Akt/mTOR autophagic pathway.ResultsIn vitro purified MEPM cells expressed cell surface markers similar to those of mouse bone marrow stem cells. Additionally, in vitro MEPM cells were ectomesenchymal and expressed the neural-crest marker human natural killer-1 (HNK-1), the mesodermal marker vimentin, and the ectodermal marker nestin. They were also positive for in vitro MEPM markers, including platelet-derived growth factor alpha (PDGFRα), ephrin B1 (Efnb1), odd-skipped related 2 (Osr2), and Meox2, as well as for stemness markers including POU class 5 homeobox 4 (Oct4), Nanog, and sex-determining region Y-related HMG box 2 (Sox2). MEPM cell pluripotency was retained through activation of the PTEN/Akt/mTOR autophagic signaling pathway. We found that atRA blocked MEPM cell pluripotency to inhibit osteogenic differentiation via miR-106a-5p targeting of PTEN mRNA and subsequent suppression of the PTEN/Akt/mTOR autophagic pathway.ConclusionsIn vitro cultured MEPM cells are ectomesenchymal stem cells that have strong osteogenic differentiation potential, and MEPM pluripotency is regulated by autophagy via the PTEN/AKT/mTOR signaling pathway. atRA disrupts MEPM cell pluripotency through PTEN/AKT/mTOR signaling inactivation where miR-106a-5p targets PTEN mRNA to reduce osteogenic differentiation of MEPM cells and results in the development of cleft palates. Our findings provide new insight into the mechanism underlying the development of cleft palate, and miR-106a-5p may act as a prenatal screening biomarker for cleft palate as well as a new diagnostic and therapeutic target.

scholarly journals Involvement of RBP4 in all-trans retinoic acid induced cleft palate

2017 ◽  
Vol 16 (5) ◽  
pp. 5915-5923 ◽  
Author(s):  
Shiyi Dong ◽  
Yadong Zhang ◽  
Hongzhang Huang
Keyword(s):  
Retinoic Acid ◽  
Cleft Palate ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid

Involvement of Smad pathway in cleft palate induced by all-trans retinoic acid

2008 ◽  
Vol 32 (3) ◽  
pp. S7-S7
Author(s):  
Yan Xu ◽  
Xiao Zhuan Liu ◽  
Xue Fei Han ◽  
Yu Jie Shi ◽  
Wen Hai Yan ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Cleft Palate ◽  
Smad Pathway ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid

DNA Methylation Changes during Cleft Palate Formation Induced by Retinoic Acid in Mice

2008 ◽  
Vol 45 (5) ◽  
pp. 545-551 ◽  
Author(s):  
Motone Kuriyama ◽  
Akikazu Udagawa ◽  
Shinya Yoshimoto ◽  
Masaharu Ichinose ◽  
Koji Sato ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Retinoic Acid ◽  
Cleft Palate ◽  
Cpg Islands ◽  
Dna Methyltransferases ◽  
Maternal Exposure ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
The Status ◽  
Polymerase Chain

Objectives: The aim of this study was to analyze epigenetic (specifically, DNA methylation) participation in the mechanisms of cleft palate only induced by maternal exposure to all-trans retinoic acid in mice. Design: Cleft palate only was induced in fetuses by maternal exposure to all-trans retinoic acid. Their secondary palates were excised for analysis. Cytosine extension assay and restriction landmark genomic scanning were performed to analyze DNA methylation status. The expression levels of the DNA methyltransferases were examined by real-time reverse transcriptase–polymerase chain reaction. Results: Using cytosine extension assay, on gestation day 14.5, the status of DNA methylation within CpG islands and in global DNA was decreased significantly in all-trans retinoic acid–treated groups compared with the controls (p < .01 and p < .05). In the controls, the status within CpG islands on gestation day 14.5 was significantly increased compared with gestation days 13.5 and 18.5 (p < .01). Using real-time reverse transcriptase–polymerase chain reaction, there was no significant change in the expression of DNA methyltransferases, except on gestation day 18.5. Using restriction landmark genomic scanning on gestation day 18.5, five spots (0.49%) in the controls and one spot (0.1%) in all-trans retinoic acid–treated groups were specifically detected. Conclusions: These results indicate that changes in DNA methylation may play an important role in the manifestation of cleft palate only caused by environmental factors such as maternal exposure to all-trans retinoic acid.

Inhibition of Smad signaling is implicated in cleft palate induced by all-trans retinoic acid

2011 ◽  
Vol 62 (2) ◽  
pp. 142-150 ◽  
Author(s):  
Yuming Wang ◽  
Yujie Dai ◽  
Xing Li ◽  
Can Chen ◽  
Wenjie Li ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Cleft Palate ◽  
Smad Signaling ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid

RNA-seq analysis of palatal transcriptome changes in all-trans retinoic acid-induced cleft palate of mice

2020 ◽  
Vol 80 ◽  
pp. 103438
Author(s):  
Yao Peng ◽  
Xin-huan Wang ◽  
Chao-nan Su ◽  
Wei-wei Qiao ◽  
Qian Gao ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Cleft Palate ◽  
Rna Seq ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid
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