Oxidative stress-induced circSOD2 inhibits osteogenesis through sponging miR-29b in metabolic-associated fatty liver disease

Figure 6 miR-29b inhibition reversed the effect of circSOD2 silencing on osteogenic differentiation of bone marrow mesenchymal stem cells. A-F: The mRNA expression of osteogenic markers, including alkaline phosphatase (ALP) (A), Runt-related transcription factor 2 (B), osteocalcin (C), and collagen type 1 alpha 1 (D), and ALP activity (E), calcium deposition (F) in bone marrow mesenchymal stem cells incubated with osteogenic medium for 7 days after cotransfection of si-circSOD2 with or without miR-29b inhibitor; G: Representative micro-computed tomography imaging of bone formation at 8 weeks in a rat calvarial critical size defect model. Rats (n = 20) were randomly assigned to four groups: Blank (Con), knockdown (Sh-circSOD2), rescue (Sh-circSOD2 + antagomiR-29b), and rescue control (Sh-circSOD2 + antagomiR-negative control); H: Trabecular bone volume per tissue volume in the rat calvarial model quantified via histomorphometric analysis (n = 5); I: Quantitative analysis of calvarial bone mineral density in the rat model (n = 5). Data indicate the mean ± SD from at least three independent experiments. Representative images are from three independent experiments. ^aP < 0.05; ^bP < 0.01; BMD: Bone mineral density; NC: Negative control; ALP: Alkaline phosphatase; RUNX2: Runt-related transcription factor 2; OCN: Osteocalcin; COL1A1: Collagen type 1 alpha 1; BMSCs: Bone marrow mesenchymal stem cells; BV/TV: Bone volume per tissue volume; Con: Control.