Title : TCDD inhibited the osteogenic differentiation of human fetal palatal mesenchymal cells through AhR and BMP-2/TGF-β/Smad signaling.

Pub. Date : 2020 Feb 15

PMID : 31887333






11 Functional Relationships(s)
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1 TCDD inhibited the osteogenic differentiation of human fetal palatal mesenchymal cells through AhR and BMP-2/TGF-beta/Smad signaling. Polychlorinated Dibenzodioxins aryl hydrocarbon receptor Homo sapiens
2 Further investigation of the underlying molecular mechanisms revealed that exposure to TCDD activated aryl hydrocarbon receptor (AhR) signaling and inhibited BMP-2/TGF-beta1/Smad pathway molecules. Polychlorinated Dibenzodioxins aryl hydrocarbon receptor Homo sapiens
3 Further investigation of the underlying molecular mechanisms revealed that exposure to TCDD activated aryl hydrocarbon receptor (AhR) signaling and inhibited BMP-2/TGF-beta1/Smad pathway molecules. Polychlorinated Dibenzodioxins aryl hydrocarbon receptor Homo sapiens
4 The inactivation of AhR signaling using CRISPR/Cas9-mediated AhR deletion or by genetic siRNA knockdown significantly blocked the effects induced by TCDD, suggesting a critical role of AhR activation in the TCDD-mediated inhibition of hFPMC osteogenic differentiation. Polychlorinated Dibenzodioxins aryl hydrocarbon receptor Homo sapiens
5 The inactivation of AhR signaling using CRISPR/Cas9-mediated AhR deletion or by genetic siRNA knockdown significantly blocked the effects induced by TCDD, suggesting a critical role of AhR activation in the TCDD-mediated inhibition of hFPMC osteogenic differentiation. Polychlorinated Dibenzodioxins aryl hydrocarbon receptor Homo sapiens
6 The inactivation of AhR signaling using CRISPR/Cas9-mediated AhR deletion or by genetic siRNA knockdown significantly blocked the effects induced by TCDD, suggesting a critical role of AhR activation in the TCDD-mediated inhibition of hFPMC osteogenic differentiation. Polychlorinated Dibenzodioxins aryl hydrocarbon receptor Homo sapiens
7 The inactivation of AhR signaling using CRISPR/Cas9-mediated AhR deletion or by genetic siRNA knockdown significantly blocked the effects induced by TCDD, suggesting a critical role of AhR activation in the TCDD-mediated inhibition of hFPMC osteogenic differentiation. Polychlorinated Dibenzodioxins aryl hydrocarbon receptor Homo sapiens
8 The inactivation of AhR signaling using CRISPR/Cas9-mediated AhR deletion or by genetic siRNA knockdown significantly blocked the effects induced by TCDD, suggesting a critical role of AhR activation in the TCDD-mediated inhibition of hFPMC osteogenic differentiation. Polychlorinated Dibenzodioxins aryl hydrocarbon receptor Homo sapiens
9 The inactivation of AhR signaling using CRISPR/Cas9-mediated AhR deletion or by genetic siRNA knockdown significantly blocked the effects induced by TCDD, suggesting a critical role of AhR activation in the TCDD-mediated inhibition of hFPMC osteogenic differentiation. Polychlorinated Dibenzodioxins aryl hydrocarbon receptor Homo sapiens
10 The cotreatment with TGF-beta1 or BMP-2 and TCDD significantly relieved the activation of AhR and rescued the impairment of osteogenesis caused by TCDD. Polychlorinated Dibenzodioxins aryl hydrocarbon receptor Homo sapiens
11 Taken together, our findings indicated that TCDD inhibited the osteogenic differentiation of hFPMCs via crosstalk between AhR and BMP-2/TGF-beta1/Smad signaling pathway. Polychlorinated Dibenzodioxins aryl hydrocarbon receptor Homo sapiens