Cux‐1 is a gene controlling G1‐S phase by repressing cyclin‐kinase inhibitors p21 and p27. CUX mice develop fibrotic damage in kidneys, testis, and liver by aberrant repression of p27. These mice showed pulmonary inflammation, vasculitis, bronchitis, bronchiectasis, and fibrosis (trichrome staining) in the bronchial basal membrane and arterial media. The heart shows inflammation, small myocardial infarctions, and a reduction of the lumen patency of coronary arteries with increase of media thickness.For fibrosis, the expression of the same conditions in lungs and heart are reported by using SMA stain. Wild type mice were controls. An average of 7 photographs at 400x were taken on both organs of each mouse.Histopathologically, with SMA1 stain, damage was present in lungs with staining in the bronchial musculature, epithelium, and media of small caliber arteries, and alveolar septa.Measurement of lumen patency of lung arteries of CUX1 mice indicated a significant reduction of their lumena. Adventitia showed fibroblasts and macrophages. The myocardium showed presence of macrophages in the myocardial fibers, coronary vasculitis with a reduced lumen patency.In conclusion, SMA1 staining, another indicator of fibrosis was seen in both lungs and heart of these mice. Differences in the thickness of these arteries, especially the adventitia was seen when SMA1 stain was compared to H&E. Little amount of collagen was seen in the coronary arteries of the mice, while present in lung vessels. No collagen was seen in the coronary arteries of controls.
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