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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, RESULTS. Meshes: Animals, Cell Proliferation, Cell Survival, Cleft Palate, In Situ Nick-End Labeling, Lymphoid Enhancer-Binding Factor 1, Mice, Microscopy, Electron, Scanning, Polychlorinated Dibenzodioxins, Wnt Signaling Pathway.
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Does 2,3,7,8-Tetrachlorodibenzo-p-dioxin Delays Palatal Shelf Elevation and suppress Wnt5a and Lymphoid Enhancing-Binding Factor 1 Signaling in Developing Palate? Context: 2,3,7,8-Tetrachlorodibenzo-p-dioxin contributes to cleft palate, but the cellular and molecular mechanisms responsible for the deleterious effect on the developing palate are unclear. Because Wnt signaling is associated with 2,3,7,8-tetrachlorodibenzo-p-dioxin in organ development, we wondered whether the malformation of the palate also results from altered Wnt signaling. The 2,3,7,8-tetrachlorodibenzo-p-dioxin administration affected cell proliferation of the anteroposterior axis of the palatal shelf and delayed shelf elevation in mice. The activity of Wnt5a and lymphoid enhancing-binding factor 1 was inhibited by 2,3,7,8-tetrachlorodibenzo-p-dioxin in the developing palate.
assistant
Downregulated Wnt5a and lymphoid enhancing-binding factor 1 are associated with 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced cleft palate. Moreover, delayed shelf elevation by 2,3,7,8-tetrachlorodibenzo-p-dioxin is the crucial mechanism contributing to the high incidence of cleft palate. Our findings may help in elucidating the mechanisms of 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced cleft palate. Final Decision: yes