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. 2019 Aug 7;14(8):e0220653. doi: 10.1371/journal.pone.0220653

Fig 4. AA regulated expression of chondrocyte and osteoblast genes at the mRNA level.

Fig 4

(A) Primary mouse articular chondrocytes were treated with AA (50 μg/mL) before RNA extraction and RT-qPCR. AA treatment significantly increased expression of immature chondrocyte genes aggrecan (AGCN) and type 2 collagen (Col2) but not mature chondrocyte differentiation marker type 10 collagen (Col10). (B) Primary mouse calvarial osteoblasts were treated with AA (50 μg/mL) before RNA extraction and RT-qPCR. AA treatment significantly increased expression of osteoblast differentiation genes alkaline phosphatase (ALP), bone sialoprotein (BSP), Indian hedgehog (Ihh), and osterix (Osx). ATDC5 chondrocytes were treated with AA before RNA extraction RT-qPCR, and no changes in (C) ER stress markers BiP or CHOP or (D) Nrf2 responsive genes Gpx2, GSR, Gsta2, or Nqo1 were observed. (E) AA treatment did not regulate expression of Jumonji family demethylases. demethylases. ATDC5 chondrocytes and MC3T3-E1 pre-osteoblasts were treated with AA before RNA extraction RT-qPCR. No significant changes in Jmjd1a or Jmjd2b were found. Results are presented as mean fold-change ± SEM. *P < 0.05 vs. control, ^P = 0.06 (Student’s t-test), n = 3–4 per group.