Over time, clinically evident pulmonary fibrosis develops.
Indeed, as reported by Yamashita and colleagues, fibrosis develops in lungs following ectopic adenoviral expression of MMP-3, and bleomycin-induced fibrosis is dramatically reduced in Mmp3−/− mice (Yamashita et al., 2011).
In nude mice, various degree of fibrosis developed around the endometrial graft.
Tubulointerstitial fibrosis developed significantly in the kidneys of acatalasemic mice group at 4 and 8 weeks after ADR administration, with significant cast formation noted at week 4.
Fibrosis developed after 6 months.
Compared to control-treated mice, silica-exposed C57BL/6 mice developed fibrosis with increased percentage of fibrosis [ Vv(f)] (Table 2, Figure 5D), lung hydroxyproline (Table 2), and apoptotic cells, identified as TUNEL positive cells (Figure S4, and Table 3).
Pharmacological manipulation of blood pressure with angiotensin II affected susceptibility as C567BL/6 mice did develop fibrosis once their blood pressure had been increased.
Finally, Lino Cardenas et al. [ 28] showed these four microRNAs, as well as miR-199a-5p miR-199a-5p miR-199a-5pAs differentoally expressed in the lungs of mice which developed fibeosis 14 damongfthe intratracheal bleomicroRNAstillation.
These findings correlate with a previous study in which mIL-8Rh knockout (KO) mice sustained higher renal bacterial burdens than did wild-type mice and eventually developed fibrosis and renal scarring (Hang et al., 2000).
In support of an anti-fibrotic role for COX-2 in lung fibrosis, COX-2-deficient mice develop increased fibrosis following bleomycin-induced injury (Keerthisingam et al., 2001).
