Open AccessLncRNA-mediated SIRT1/FoxO3a and SIRT1/p53 signaling pathways regulate type II alveolar epithelial cell senescence in patients with chronic obstructive pulmonary disease
Author(s) -
Chao Gu,
Yaqing Li,
Jialiang Li,
Xiwang Ying,
Yuanshun Liu,
Jianping Yan,
Chun Chen,
Hongbin Zhou,
Liming Cao,
Yingyu Ma
Publication year - 2017
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2017.6367
Subject(s) - senescence , sirtuin 1 , copd , sirtuin , biology , downregulation and upregulation , cell cycle , cell , lung , cancer research , pathogenesis , microbiology and biotechnology , immunology , medicine , gene , genetics , acetylation
The loss of alveolar structure and airspace enlargement are major pathological changes in chronic obstructive pulmonary disease (COPD). Type II alveolar epithelial cells (AECII) are involved in maintaining lung tissue repair and alveolar homeostasis. Long non‑coding RNAs (lncRNAs) are involved in multi‑regulating gene transcription, affecting processes including embryonic development, cell differentiation and cellular senescence. The primary aim of the present study was to explore the mechanisms of AECII senescence regulated by lncRNA‑mediated sirtuin 1 (SIRT1) and forkhead box O 3a (FoxO3a) signaling pathways in patients with COPD. Lung tissues from patients with COPD exhibited pathological characteristics and significantly increased senescence‑associated β‑galactosidase activity. Furthermore, the expression levels of senescence‑associated lncRNA1 (SAL‑RNA1), SIRT1 and FoxO3a were reduced, but SAL‑RNA2, SAL‑RNA3, p53 and p21 were upregulated in the lung tissues of patients with COPD compared with control. The results of the present study indicated that lncRNA‑mediated SIRT1/p53 and FoxO3a signaling pathways may regulate AECII senescence in the pathogenesis of COPD, which may provide a novel experimental basis for the treatment of COPD.