Fig. 6

CSE impairs bone remodeling mediated by the NFκB pathway. The supernatants collected from differentiated BMSCs treated with CSE at concentrations as indicated. Bone marrow plasma collected from non-smoke and smoke-exposed mice. The TNFα levels of the supernatants (a) and bone marrow plasma (b) were measured by ELISA. Smoke exposure significantly increased TNFα expression. Consistently, CSE increased the levels of TNFα in BMSCs. c The supernatants collected from QNZ treated BMSC w/o 1% CSE. TNFα levels were significantly decreased. b Identification of DNA binding activity of CSE-regulated transcriptional factors using EMSA. The BMSC cells were treated with CSE, and nuclear proteins were extracted and incubated with [-³²P]-labeled NFκB probe in the presence or absence of anti-p65 antibody or anti-cyclin D1 antibody. CSE induced the NFκB-p65 complex formation as evidenced by a gel shift using anti-cyclin D1 antibody. e Nuclear proteins were extracted from BMSCs that were derived from non-smoke and smoke mice and incubated with labeled probes. Smoke exposure increased NFκB binding activity but not AP-1 binding activity. ^*P < 0.05 compared to vehicle or non-smoke group; ^**P < 0.001 compared to the vehicle; ^†,#P < 0.01 compared to vehicle. All the data are from 3 independent experiments