Published online Aug 26, 2023. doi: 10.4252/wjsc.v15.i8.807
Peer-review started: March 28, 2023
First decision: June 25, 2023
Revised: June 29, 2023
Accepted: July 14, 2023
Article in press: July 14, 2023
Published online: August 26, 2023
Processing time: 149 Days and 21.6 Hours
Bone marrow mesenchymal stromal cells (BMSCs) are one of the most commonly used seed cells in bone tissue engineering. Aryl hydrocarbon receptor (AhR) has been recognized as a nuclear receptor that modulates bone turnover. However, the function of constitutive AhR in BMSCs remains unclear.
To explore whether AhR is involved in the regenerative potential of mouse BMSCs (mBMSCs).
To investigate the role of AhR in the osteogenic and macrophage-modulating potential of mBMSCs and the underlying mechanism.
Immunochemistry and immunofluorescent staining were used to observe the expression of AhR in mouse bone marrow tissue and mBMSCs. The overexpression or knockdown of AhR was achieved by lentivirus-mediated plasmid. The osteogenic potential was observed by alkaline phosphatase and alizarin red staining. The mRNA and protein levels of osteogenic markers were detected by quantitative polymerase chain reaction and western blot. After coculture with different mBMSCs, the cluster of differentiation (CD) 86 and CD206 expressions levels in RAW 264.7 cells were analyzed by flow cytometry. To explore the underlying molecular mechanism, the interaction of AhR with signal transducer and activator of transcription 3 (STAT3) was observed by co-immunoprecipitation and phosphorylation of STAT3 was detected by western blot.
AhR expressions in mouse bone marrow tissue and isolated mBMSCs were detected. AhR overexpression enhanced the osteogenic potential of mBMSCs while AhR knockdown suppressed it. The ratio of CD86+ RAW 264.7 cells cocultured with AhR-overexpressed mBMSCs was reduced and that of CD206+ cells was increased. AhR directly interacted with STAT3. AhR overexpression increased the phosphorylation of STAT3. After inhibition of STAT3 via stattic, the promotive effects of AhR overexpression on the osteogenic differentiation and macrophage-modulating were partially counteracted.
AhR plays a beneficial role in the regenerative potential of mBMSCs partially by increasing phosphorylation of STAT3.
This study suggested that AhR and its interaction with STAT3 might be a potential candidate target for achieving optimal bone regeneration in mBMSCs-based tissue engineering.