Former studies have shown that acute exposure to cigarette smoke in the mouse lung induces a loss of activity of SLPI [ 22], while chronic smoke exposure increased SLPI expression in the smoke-exposed mice [ 23].
Strain PR8 is highly adapted to growth in mouse lung and induces interstitial pneumonia [25], [26], similar to that observed in human cases of viral pneumonia.
Moreover, conditional deletion of BMPR1A, which is normally expressed during branching morphogenesis in the mouse lung epithelium, induces defects in lung development, marked by increased apoptosis and morphological changes [11].
The mouse lung tumors were induced using 3-methylcholanthrene-butylated hydroxytoluene (MCA-BHT).
Mouse lung carcinogenesis was induced by NNK in the susceptible A/J mice as described previously [ 19].
As predicted, introduction of complementary LNAs stabilizes sense and antisense nc-rRNAs in mouse lung cells and induces cell death.
Since it has been shown that lungs with pre-existing injury are more susceptible to the effects of MV [25],[26], we randomized in a second set of experiments WT and KO mice with pre-injured lungs (induced by inhalation of 5 μg LPS (Escherichia coli L4130, Sigma Aldrich, St . Louis MO, USA) 1 h before randomization) to the above described ventilation strategies or spontaneously breathing for 5 h.
2014), while disruption of two mce1 genes within this operon, namely, mce1A or yrbE1B, similarly caused faster replication in mice lungs, hypervirulence, induced poor granuloma formation and a reduced proinflammatory response (Shimono et al. 2003; Joshi et al. 2006).
However, it has been reported that in the adult mouse lung, β-catenin was induced during ATII cell to ATI cell transdifferentiation in normoxia condition [93, 94].
