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. Author manuscript; available in PMC: 2009 Sep 23.
Published in final edited form as: Circulation. 2009 Apr 20;119(17):2313–2322. doi: 10.1161/CIRCULATIONAHA.108.782458

Figure 7.

Figure 7

Overexpression of the inhibitory subunit IκBα attenuates NF-κB–mediated TRPC6 expression and inhibits agonist-mediated Ca2+ influx in IPAH-PASMC. A, Overexpression of IκBα (Ad-IκB) inhibits translocation of NF-κB p50 and p65 into the nucleus (left) and diminishes TNF-α–stimulated TRPC6 expression (right). GAPDH, histone (H2A), and p84 antibodies were used as controls for nuclear and cytoplasmic proteins. Experiments were reproduced 3 times. B, Summarized results showing that TNF-α increases the resting [Ca2+]cyt (left) and enhanced OAG-induced [Ca2+]cyt rise (right) in IPAH PASMCs (−254C/G), whereas IκBα (Ad-IκB) abolishes the TNF-α–mediated enhancement of the resting [Ca2+]cyt and OAG-mediated Ca2+ influx. C, Summarized results showing that TNF-α negligibly affects the resting [Ca2+]cyt (left) and OAG-induced [Ca2+]cyt increase (right) in normal PASMCs (−254C/C).