Figure 7.

MiR-181d regulates the Adamts1-ECM-FAK–ERK axis. (a) C3H10T1/2 cells infected with MSCV-miR-181d or/and MSCV-Adamts1 were treated with BMP4 (10 ng/ml) until postconfluent, cell lysis were subjected to SDS-PAGE to analyze the Adamts1 protein expression, with Hsp90 as a loading control. (b and c) After reaching postconfluence, the cells were induced to differentiate into adipocytes (MDI). The effects of miR-181d or/and Adamts1 overexpression on adipocyte lineage commitment and subsequent differentiation were assessed at day 6 by Oil Red O staining and 422/aP2 protein expression. (d) C3H10T1/2 cells incubated with miR-181d inhibitor or/and Adamts1 siRNA were treated with BMP4 (10 ng/ml) until postconfluent, cell lysis were subjected to SDS-PAGE to analyze the Adamts1 protein expression, with Hsp90 as a loading control. (e and f) After reaching postconfluence, the cells were induced to differentiate into adipocytes (MDI). The effects of miR-181d inhibitor or/and Adamts1 siRNA on adipocyte lineage commitment and subsequent differentiation were assessed at day 6 by Oil Red O staining and 422/aP2 protein expression. (g–j) Western blots of postconfluent cell lysates were probed with the indicated antibodies, with Hsp90 used as a loading control