European review for medical and pharmacological sciences · 2017
MiR-145 silencing promotes steroid-induced avascular necrosis of the femoral head repair via upregulating VEGF.
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Tian Z-J, Liu B-Y, Zhang Y-T, Chen X-Z, Qiao G-Y, Wang S, Ma Z-L
Аннотация
OBJECTIVE: To investigate the role of miR-145 silencing in the expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), B-cell lymphoma-2 (Bcl-2), BCL2-Associated X(bax) and caspase-3 in avascular necrosis of femoral head (ANFH).
MATERIALS AND METHODS: A total of 12 healthy wild-types (the control group) and 12 miR-145 knock-out (miR-145-/-) (the experimental group) adult New Zealand white rabbits were selected to construct ANFH model with a steroid. Four weeks later, immunohistochemistry, qRT-PCR and Western blot were performed to measure the VEGF, bFGF, Bcl-2, bax, caspase-3, β-catenin as well as c-Myc expression. Terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining analysis was used to detect the apoptosis of bone cells in each group.
RESULTS: Compared with the control group, the expression of VEGF, bFGF, Bcl-2, β-catenin and c-Myc in the miR-145-/- group raised (p<0.05). Moreover, the expression level of bax and caspase-3 significantly decreased in the miR-145-/- group (p<0.05). TUNEL staining showed decreased apoptosis in the miR-145-/- group.
CONCLUSIONS: MiR-145 silencing promotes bone repair of ANFH via upregulating VEGF, bFGF and inhibiting the bone cells apoptosis through Wnt/β-catenin pathway.
MATERIALS AND METHODS: A total of 12 healthy wild-types (the control group) and 12 miR-145 knock-out (miR-145-/-) (the experimental group) adult New Zealand white rabbits were selected to construct ANFH model with a steroid. Four weeks later, immunohistochemistry, qRT-PCR and Western blot were performed to measure the VEGF, bFGF, Bcl-2, bax, caspase-3, β-catenin as well as c-Myc expression. Terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining analysis was used to detect the apoptosis of bone cells in each group.
RESULTS: Compared with the control group, the expression of VEGF, bFGF, Bcl-2, β-catenin and c-Myc in the miR-145-/- group raised (p<0.05). Moreover, the expression level of bax and caspase-3 significantly decreased in the miR-145-/- group (p<0.05). TUNEL staining showed decreased apoptosis in the miR-145-/- group.
CONCLUSIONS: MiR-145 silencing promotes bone repair of ANFH via upregulating VEGF, bFGF and inhibiting the bone cells apoptosis through Wnt/β-catenin pathway.