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. 2020 Aug;8(16):1009. doi: 10.21037/atm-20-5307

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2020 Annals of Translational Medicine. All rights reserved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0.

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TMAO promotes the adipogenic differentiation and inhibits the osteogenic differentiation of BMSCs. (A) Adipogenic differentiation was detected by oil red O staining; (B) osteogenic differentiation was detected by alizarin red staining; (C) the expressions of NF-κB, PPARγ, C/EBP-α, Runx2 and OPN in BMSCs were measured by WB. Actin was used as an internal control; (D) quantification of NF-κB/Actin, PPARγ/Actin, C/EBP-α/Actin, Runx2/Actin, and OPN/Actin protein expression. *, P<0.05, **, P<0.01, ***, P<0.001 vs. OIM or AIM group. TMAO, trimethylamine N-oxide; BMSCs, bone marrow mesenchymal stem cells. NF-κB, nuclear factor-κB; PPARγ, Peroxisome proliferator-activated receptor gamma; C/EBP-α, CCAAT/enhancer-binding protein alpha; Runx2, runt-related transcription factor 2; OPN, Osteopontin.