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. 2012 Dec;181(6):2038–2046. doi: 10.1016/j.ajpath.2012.08.040

Figure 5.

Figure 5

The proteasome is responsible for IFN-γ–induced degradation of MyHC in NRVMs. A: Proteasome activity in NRVMs treated with vehicle (control), IFN-γ, or bortezomib for 24 or 48 hours. Bars are normalized to control at each time point. B: Quantification of proteolytic activity after inhibition of the proteasome in NRVMs treated with MG-132 or vehicle, normalized to vehicle-treated NRVMs. C: Top panel: Representative myofibrillar gels of protein lysates from NRVMs treated with vehicle (C) or IFN-γ and vehicle (dimethyl sulfoxide, DMSO) or MG-132. The MyHC band is as indicated. Bottom panel: Densitometric quantification of MyHC. Values are normalized to vehicle-treated cells. D: Top panel: Representative images of NRVMs treated with vehicle or IFN-γ in the presence or absence of bortezomib. Cells were immunolabeled with antibodies raised against α-actinin. Bottom panel: Quantification of the NRVM area, indicated as arbitrary units. E: Immunoproteasome activity in NRVMs treated with vehicle (control), IFN-γ, or bortezomib for 24 or 48 hours. Bars are normalized to control at each time point. F: Quantification of expression of atrogin-1 or MuRF-1 normalized to 18S in NRVMs treated with IFN-γ for 24 or 48 hours. All values are normalized to expression in vehicle-treated myocytes. *P < 0.05, **P < 0.01, and ***P < 0.001 compared with control or as indicated. †P < 0.001 compared with the respective no drug samples.