Activation of Notch1 inhibits medial edge epithelium apoptosis in all-trans retinoic acid-induced cleft palate in mice

Zhang, Yadong; Dong, Shujun; Wang, Weicai; Wang, Jianning; Wang, Miao; Chen, Mu; Hou, Jinsong; Huang, Hongzhang

doi:10.1016/j.bbrc.2016.06.107

Cited by 10 publications

(8 citation statements)

References 30 publications

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“…Protein derived from cultured HEPM cells was also detected by western blotting. The following steps were repeated as described previously ( 15 ). In addition to the antibodies mentioned above, the following antibodies were used: Rabbit monoclonal anti-extracellular signal-related kinase (ERK) 1/2 (cat.…”

Section: Methodsmentioning

confidence: 99%

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

Dong

Zhang

Huang

2017

Molecular Medicine Reports

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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 (E10.0). Control groups were given the equivalent volume of corn oil. Pregnant mice were dissected at E12.5, E13.5 and E14.5 to obtain the embryonic palates. The expression levels of RBP4 in the embryonic palatal mesenchyme (EPM) were determined by immunohistochemistry, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting. Human embryonic palatal mesenchymal cells were exposed to atRA to detect the variation in RBP4 induced by atRA in vitro. Small interfering RNA was used to suppress the expression of RBP4, and a plasmid overexpressing RBP4 was used to examine upregulated expression. The cell counting kit-8 assay was used to evaluate the effect of RBP4 on cell proliferation. The expression levels of p27 and cyclin D1 were determined by RT-qPCR and western blotting, while the expression levels of extracellular signal-related kinase (ERK) 1/2 and protein kinase B (AKT) were assessed by western blotting. At E14.5, RBP4 was strongly expressed in the EPM, while it was downregulated following atRA treatment, which induced cleft palate in vivo. In vitro experiments indicated that atRA suppressed the expression of RBP4 and altered the expression of p27 and cyclin D1 to cause growth inhibition. Knockdown of RBP4 resulted in decreased expression of cyclin D1 and increased p27, and suppressed proliferation. Overexpression of RBP4 reversed the inhibitory effect of atRA and promoted proliferation via the ERK1/2 and AKT signaling pathways. These results suggested that RBP4 was involved in cleft palate induced by atRA and it can be suppressed by atRA to cause growth inhibition in the embryonic palate.

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Section: Methodsmentioning

confidence: 99%

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

Dong

Zhang

Huang

2017

Molecular Medicine Reports

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“…Additionally, ATRA exposure can modulate Notch signaling in palatal epithelial and mesenchymal cells, possibly affecting p21 signaling in both tissues. One study showed that ATRA exposure at embryonic day (E) 12 increased the abundance of Notch1 in MEE cells at E15, which was hypothesized to inhibit normal apoptotic processes (Y. D. Zhang et al, 2016). Another study found that ATRA exposure at E10 increased the abundance of Notch2 and decreased that of CyclinD1 in mesenchymal cells between E12.5 and 14.5, thereby inhibiting proliferation (Y. D. Zhang et al, 2017).…”

Section: Environmental Signaling Pathways In Orofacial Cleftsmentioning

confidence: 99%

Environmental mechanisms of orofacial clefts

Garland

Reynolds

Zhou

2020

Birth Defects Research

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Orofacial clefts (OFCs) are among the most common birth defects and impart a significant burden on afflicted individuals and their families. It is increasingly understood that many nonsyndromic OFCs are a consequence of extrinsic factors, genetic susceptibilities, and interactions of the two. Therefore, understanding the environmental mechanisms of OFCs is important in the prevention of future cases. This review examines the molecular mechanisms associated with environmental factors that either protect against or increase the risk of OFCs. We focus on essential metabolic pathways, environmental signaling mechanisms, detoxification pathways, behavioral risk factors, and biological hazards that may disrupt orofacial development.

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“…For example, it was demonstrated that LacZ + cells from the Rosa26-lacZ mouse exhibited preferential migration in the nasal and posterior directions into the opposing LacZ − shelf during MES fusion (Jin and Ding 2006). More recently, murine PS cultures have incorporated the ever-expanding, molecular-genetic toolkit, including fluorescent reporters, genetic manipulation, and live-imaging that allow for a unique opportunity to rapidly study palatal closure (Jin and Ding 2006;Ke et al 2015;Zhang et al 2016;Narhi 2017).…”

Section: Ex Vivo Palate Culturesmentioning

confidence: 99%

Closing the Gap: Mouse Models to Study Adhesion in Secondary Palatogenesis

et al. 2017

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Secondary palatogenesis occurs when the bilateral palatal shelves (PS), arising from maxillary prominences, fuse at the midline, forming the hard and soft palate. This embryonic phenomenon involves a complex array of morphogenetic events that require coordinated proliferation, apoptosis, migration, and adhesion in the PS epithelia and underlying mesenchyme. When the delicate process of craniofacial morphogenesis is disrupted, the result is orofacial clefting, including cleft lip and cleft palate (CL/P). Through human genetic and animal studies, there are now hundreds of known genetic alternations associated with orofacial clefts; so, it is not surprising that CL/P is among the most common of all birth defects. In recent years, in vitro cell-based assays, ex vivo palate cultures, and genetically engineered animal models have advanced our understanding of the developmental and cell biological pathways that contribute to palate closure. This is particularly true for the areas of PS patterning and growth as well as medial epithelial seam dissolution during palatal fusion. Here, we focus on epithelial cell-cell adhesion, a critical but understudied process in secondary palatogenesis, and provide a review of the available tools and mouse models to better understand this phenomenon.

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Activation of Notch1 inhibits medial edge epithelium apoptosis in all-trans retinoic acid-induced cleft palate in mice

Cited by 10 publications

References 30 publications

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

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

Environmental mechanisms of orofacial clefts

Closing the Gap: Mouse Models to Study Adhesion in Secondary Palatogenesis

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