Constitutive aryl hydrocarbon receptor facilitates the regenerative potential of mouse bone marrow mesenchymal stromal cells

Figure 6 The molecular mechanism of the role of aryl hydrocarbon receptor in osteogenic differentiation and macrophage-modulating in mouse bone marrow mesenchymal stromal cells. A: Co-immunoprecipitation assay showed that aryl hydrocarbon receptor (AhR) and signal transducer and activator of transcription 3 (STAT3) directly interacted in mouse bone marrow mesenchymal stromal cells (mBMSCs); B: Western blot lanes demonstrated that AhR overexpression promoted phosphorylation of STAT3 compared to negative control, while AhR knockdown suppressed it; C: The specific STAT3 inhibitor stattic (2 mmol/L) partially alleviated the promoted STAT3 phosphorylation by AhR overexpression; D: Alkaline phosphatase (upper) and alizarin red staining (lower) staining indicated that 2 mmol/L stattic partially inhibited the elevated osteogenic potential by AhR overexpression; E and F: The histograms of flow cytometry and quantitative analysis manifested that 2 mmol/L stattic partially reversed the CD86 inhibition and CD206 promotion in RAW 264.7 by conditioned medium from overexpression-AhR mBMSCs. AhR: Aryl hydrocarbon receptor; oe-NC: Overexpression-negative control; oe-AhR: Overexpression-AhR; sh-NC: Knockdown-negative control; sh-AhR: Knockdown-AhR; STAT3: Signal transducer and activator of transcription 3; p-STAT3: Phosphorylated STAT3; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase.