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. Author manuscript; available in PMC: 2011 Dec 1.
Published in final edited form as: J Mol Med (Berl). 2011 Feb 12;89(6):577–593. doi: 10.1007/s00109-011-0732-8

Fig. 7.

Fig. 7

Increased VCP expression in cigarette smoke (CS)-exposed murine lungs correlates with stress response and apoptosis. The age- and sex-matched WT mice (n=3, each group) were exposed to 3- (a) or 5-day CS (b). The immunostainings of longitudinal lung sections show a significant increase (p<0.001) in VCP, nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB), NOS2, and p-eIF2α expression levels and accumulation of poly-ubiquitinated (Ub) proteins in lungs of CS-induced mice (a). The extent of inflammation (a) and number of apoptotic cells (b TUNEL staining) were also elevated in the lungs of CS-exposed mice. Scale=50 µm. c The age- and sex-matched WT mice (n=3) were exposed to CS for 4 weeks (sub-chronic exposure). The immunoblotting of lung total-protein lysates demonstrate a significant (p<0.05) increase in VCP and NFκB expression in the sub-chronic CS-exposed murine lungs as compared with air. β-Actin was used as a loading control. The data verify the correlation of VCP expression to ubiquitin accumulation, inflammatory-oxidative stress and apoptosis in response to acute or sub-chronic CS exposure in murine lungs