Fig. 3

Mitochondrial function is required for the cementoblastic differentiation of PDLSCs in either noninflammatory or inflammatory environments. a–c Mitochondrial dysfunction impairs the cementoblastic differentiation of PDLSCs. The cells were incubated in medium with EMD (noninflammatory environment). a Relative cementoblastic differentiation-related gene expression levels of BSP, CAP and CEMP-1 in the PDLSCs without (control) or with pretreatment with 10 μmol·L⁻¹ H₂O₂ (H₂O₂) or 10 μg·mL⁻¹ Oligo (Oligo) for 24 h (qRT-PCR). b Relative cementoblastic differentiation-related protein expression of BSP, CAP and CEMP-1 in the PDLSCs without (control) or with pretreatment with 10 μmol·L⁻¹ H₂O₂ (H₂O₂) or 10 μg·mL⁻¹ Oligo (Oligo) for 24 h (Western blot). c Semiquantitative analysis of the protein expression levels (normalized to β-actin) in terms of relative gray density. d–f Reversing inflammation-induced mitochondrial dysfunction rescued the cementoblastic differentiation of PDLSCs. The cells were incubated in medium with both inflammatory cytokines and EMD (inflammatory environment). d Relative cementoblastic differentiation-related gene expression levels of BSP, CAP and CEMP-1 in the PDLSCs without (control) or with pretreatment with 1 mmol·L⁻¹ NAC (NAC) or 20 nmol·L⁻¹ Visomitin (Visomitin) for 2 h (qRT-PCR). e Relative cementoblastic differentiation-related protein expression of BSP, CAP and CEMP-1 in the PDLSCs without (control) or with pretreatment with 1 mmol·L⁻¹ NAC (NAC) or 20 nmol·L⁻¹ Visomitin (Visomitin) for 2 h (Western blot). f Semiquantitative analysis of protein expression levels (normalized to β-actin) in terms of relative gray density. The data are shown as the mean ± SD for n from 6 to 9; *P < 0.05, **P < 0.01 and ***P < 0.001 indicate significant differences between the indicated columns