Fig. 3: Spi-C regulates osteoclast marker gene expression.
From: Spi-C positively regulates RANKL-mediated osteoclast differentiation and function
a, b BMMs transfected with a scrambled nontargeting siRNA (siCon) or Spi-C siRNA (siSpi-C) were cultured without or with RANKL for 24 h a or 5 days b. Then, qPCR a or western blot analysis b was performed. c BMMs infected with an empty lentiviral vector (EV) or Spi-C-expressing lentiviral vector (Spi-C) were cultured without or with RANKL (200 ng/ml) for 24 h, and qPCR was performed. d Isolated BMMs infected with control shRNA lentiviral vector (shCon) or Spi-C shRNA expression lentiviral vector (shSpi-C) were cultured without or with RANKL (200 ng/ml) for 48 h, and qPCR was performed. e BMMs infected with empty lentiviral vector (EV) or Spi-C-expressing lentiviral vector (Spi-C) were cultured without or with RANKL (200 ng/ml) for 48 h, and qPCR was performed. The data are presented as the mean ± SD of three independent experiments. *p < 0.05, **p < 0.005 vs. untreated cells and #p < 0.05, ##p < 0.005 vs. RANKL-treated cells.
