Figure 3.
Figure 3. Knockdown of BMPRII reduces BMP-2–mediated proliferation and survival of hPAECs but enhances their migratory response. (A) Western immunoblots for BMPRII and α-tubulin in hPAECs nucleofected with nontargeting control (CON RNAi) and BMPRII siRNA (BMPRII RNAi). Error bars denote mean ± SEM for three different assessments. ***, P < 0.0001 (vs. nontargeting control). (B) TOPflash activity assay. **, P < 0.001 (vs. nontargeting control); ##, P < 0.001 (vs. BMP-2–stimulated nontargeting control). (C–E) Cell proliferation (C), caspase 3/7 activity (D), and cell migration (E) assays using cells nucleofected with nontargeting or BMPRII-specific siRNA as in Fig. 1. (B–E) Error bars represent mean ± SEM from three different experiments performed in triplicate. *, P < 0.01 and **, P < 0.001 (vs. unstimulated nontargeting control); ##, P < 0.001 (vs. BMP-2– or Wnt3a–stimulated nontargeting control).

Knockdown of BMPRII reduces BMP-2–mediated proliferation and survival of hPAECs but enhances their migratory response. (A) Western immunoblots for BMPRII and α-tubulin in hPAECs nucleofected with nontargeting control (CON RNAi) and BMPRII siRNA (BMPRII RNAi). Error bars denote mean ± SEM for three different assessments. ***, P < 0.0001 (vs. nontargeting control). (B) TOPflash activity assay. **, P < 0.001 (vs. nontargeting control); ##, P < 0.001 (vs. BMP-2–stimulated nontargeting control). (C–E) Cell proliferation (C), caspase 3/7 activity (D), and cell migration (E) assays using cells nucleofected with nontargeting or BMPRII-specific siRNA as in Fig. 1. (B–E) Error bars represent mean ± SEM from three different experiments performed in triplicate. *, P < 0.01 and **, P < 0.001 (vs. unstimulated nontargeting control); ##, P < 0.001 (vs. BMP-2– or Wnt3a–stimulated nontargeting control).

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