Alveolar Epithelial Cells Express Markers of Senescence in Lungs from Patients With Idiopathic Pulmonary Fibrosis
의약학 > 내과학
( Eun Kyung Kim ) , ( Seung Ick Cha ) , ( Aaron V Schroeder ) , ( Jasleen Kukreja ) , ( Kirk D Jones ) , ( Jeffrey A Golden ) , ( Michael A Matthay ) , ( David J Erle ) , ( Harold R Collard ) , ( Paul J Wolters )
대한결핵 및 호흡기학회
대한결핵및호흡기학회 추계학술발표초록집 2012년, 제114권 247(총1페이지)
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    Background: The prevalence of idiopathic pulmonary fibrosis (IPF) increases with age. Recent reports have demonstrated that mutations in TERT or TERC and short telomeres are risk factors for the development of IPF. Because short telomeres induce cellular senescence, these findings suggest senescence may occur in IPF lung. Methods: To evaluate for cellular senescence, we compared microRNA (miRNA) expression by miRNA arrays in type II epi-thelial cells. Senescence-associated β-galactosidase staining and immunohistochemical detection of p16, p21 and p53 were examined in sections of lung obtained from IPF patients and normal controls. Results: Expression of miR34-a, -b, and -c, which reportedly induce senescence in human epithelial cells are increased in IPF type II epithelial cells. β-Galactosidase activity is detectable on type II epithelial cells of IPF, but not normal lung. p16, p21 and p53 were detectable by immunostaining in IPF epithelial cells. Conclusions: IPF epithelial cells express several markers of senescence. These results suggest that the senescence of alveolar epithelial cells is accelerated in patients with IPF and may play a role in the pathogenesis of IPF.
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