兰州大学机构库
Retinoic acid delays murine palatal shelf elevation by inhibiting Wnt5a-mediated noncanonical Wnt signaling and downstream Cdc-42/F-actin remodeling in mesenchymal cells
Ma, Yan-Qing1,2; Zhang, Xin-Yu1,2; Zhao, Shi-Wei1,2; Li, Dou1,2; Cai, Min-Qin1,2; Yang, Hui1,2; Wang, Xiao-Ming1,2; Xue, Hui3
2023-10-15
Online publication date2023-09
Source PublicationBirth Defects Research   Impact Factor & Quartile Of Published Year  The Latest Impact Factor & Quartile
ISSN2472-1727
Volume115Issue:17Pages:1658-1673
page numbers16
AbstractBackground: Mammalian palatal shelves erupted from maxillary prominences undergo vertical extention, transient elevation, and horizontal growth to fuse. Previous studies in mice reported that the retinoic acid (RA) contributed to cleft palate in high incidence by delaying the elevating procedure, but little was known about the underlying biological mechanisms. Methods: In this study, hematoxylin-eosin and immunofluorescence staining were employed to evaluate the phenotypes and the expression of related markers in the RA-treated mice model. In situ hybridization and RT-qPCR were used to detect the expression of genes involved in Wnt signaling pathway. The palatal mesenchymal cells were cultured in vitro, and stimulated with RA or CASIN, and co-treated with Foxy5. Wnt5a and Ccd42 expression were evaluated by immunofluorescence staining. Phalloidin was used to label the microfilament cytoskeleton (F-actin) in cultured cells. Results: We revealed that RA resulted in 100% incidence of cleft palate in mouse embryos, and the expression of genes responsible for Wnt5a-mediated noncanonical Wnt signal transduction were specifically downregulated in mesenchymal palatal shelves. The in vitro study of palatal mesenchymal cells indicated that RA treatment disrupted the organized remodeling of cytoskeleton, an indicative structure of cell migration regulated by the small Rho GTPase Cdc42. Moreover, we showed that the suppression of cytoskeleton and cell migration induced by RA was partially restored using the small molecule Foxy-5-mediated activation of Wnt5A, and this restoration was attenuated by CASIN (a selective GTPase Cdc42 inhibitor) again. Conclusions: These data identified a crucial mechanism for Wnt5a-mediated noncanonical Wnt signaling in acting downstream of Rho GTPase Cdc42 to regulate cytoskeletal remodeling and cell migration during the process of palate elevation. Our study provided a new explanation for the cause of cleft palate induced by RA.
Keywordcleft palate cytoskeleton retinoic acid Rho GTPase Wnt signaling
PublisherWILEY
DOI10.1002/bdr2.2244
Indexed BySCIE
Language英语
WOS Research AreaDevelopmental Biology ; Toxicology
WOS SubjectDevelopmental Biology ; Toxicology
WOS IDWOS:001063347000001
Original Document TypeArticle
PMID 37675882
Citation statistics
Document Type期刊论文
Identifierhttps://ir.lzu.edu.cn/handle/262010/568809
Collection兰州大学
Corresponding AuthorWang, Xiao-Ming; Xue, Hui
Affiliation
1.Lanzhou Univ, Sch Stomatol, Key Lab Dent Maxillofacial Reconstruct & Biol Inte, Lanzhou 730000, Gansu, Peoples R China;
2.Lanzhou Univ, Sch Stomatol, Dept Orthodont, Lanzhou 730000, Gansu, Peoples R China;
3.Nanjing Med Univ, Affiliated Suzhou Hosp, Suzhou Municipal Hosp, Gusu Sch,Dept Stomatol, Suzhou, Jiangsu, Peoples R China
Recommended Citation
GB/T 7714
Ma, Yan-Qing,Zhang, Xin-Yu,Zhao, Shi-Wei,et al. Retinoic acid delays murine palatal shelf elevation by inhibiting Wnt5a-mediated noncanonical Wnt signaling and downstream Cdc-42/F-actin remodeling in mesenchymal cells[J]. Birth Defects Research,2023,115(17):1658-1673.
APA Ma, Yan-Qing.,Zhang, Xin-Yu.,Zhao, Shi-Wei.,Li, Dou.,Cai, Min-Qin.,...&Xue, Hui.(2023).Retinoic acid delays murine palatal shelf elevation by inhibiting Wnt5a-mediated noncanonical Wnt signaling and downstream Cdc-42/F-actin remodeling in mesenchymal cells.Birth Defects Research,115(17),1658-1673.
MLA Ma, Yan-Qing,et al."Retinoic acid delays murine palatal shelf elevation by inhibiting Wnt5a-mediated noncanonical Wnt signaling and downstream Cdc-42/F-actin remodeling in mesenchymal cells".Birth Defects Research 115.17(2023):1658-1673.
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