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( Jong Sun Park ),( Jasmine Lee ),( Ram P. Naikawadi ),( Gary Green ),( Paul Wolters ) 대한결핵 및 호흡기학회 2020 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.128 No.-
Purpose Telomere maintenance dysfunction has been implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF) and short telomere length (TL) is associated with worse survival in IPF. However, it is unknown whether telomere dysfunction is associated with pathogenesis of idiopathic nonspecific interstitial pneumonia (iNSIP). The purpose of this study was to determine whether TL is shortened in alveolar type 2 epithelial (AT2) cells of iNSIP. Methods Idiopathic NSIP were diagnosed at the University of California San Francisco and healthy control lungs were obtained from unused donor lungs. Fluorescence in situ hybridization (FISH) was performed in formalin fixed and paraffin embedded (FFPE) section of lungs. Telomeres were labeled with a telomere-Cy3 PNA probe and AT2 cells were labeled with surfactant protein C (SPC). Telomere fluorescent signal was quantified using the MetaMorph software. Results Age-matched 22 lung tissues (11 iNSIPs, 11 healthy controls) were used to measure TL. Age of the subjects ranges from 31 to 72. Representative FISH images of iNSIP and normal lungs were shown in Figure 1 (A: normal, B:iNSIP). Telomere signal had a tendency to decrease as age increase. However, there was no significant difference in TL of AT2 cells (median FISH-TL signal 11.5 vs. 13.0, p = 0.949) between iNSIP and normal lungs. Conclusion The telomere length was not shorter in the AT2 cells of iNSIP compared to healthy controls. Further study is needed to investigate the role of telomere in iNSIP.
( 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 2012 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.114 No.-
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.