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Klotho Regulates Cigarette Smoke-Induced Autophagy: Implication in Pathogenesis of COPD
Authors:Lingling?Li  mailto:illl@.com"   title="  illl@.com"   itemprop="  email"   data-track="  click"   data-track-action="  Email author"   data-track-label="  "  >Email author,Min?Zhang,Liqin?Zhang,Yusheng?Cheng,Xiongwen?Tu,Zhiwei?Lu  mailto:sduzhiwei@sina.com"   title="  sduzhiwei@sina.com"   itemprop="  email"   data-track="  click"   data-track-action="  Email author"   data-track-label="  "  >Email author
Affiliation:1.Department of Respiratory Medicine, Yijishan Hospital,Wannan Medical College,Wuhu,China;2.Department of Emergency, Yijishan Hospital,Wannan Medical College,Wuhu,China
Abstract:

Introduction

Chronic obstructive pulmonary disease is a progressive lung disease characterized by abnormal cellular responses to cigarette smoke, resulting in tissue destruction and airflow limitation. Autophagy is a fundamental cellular process that eliminates long-lived proteins and damaged organelles through lysosomal degradation pathway, though its role in human diseases remains unclear. We hypothesized that an anti-aging protein, Klotho plays an important role in regulating autophagy in response to cigarette smoke (CS).

Methods

Autophagy was measured by detecting LC3-I and LC3-II expressions. The regulation of autophagy expression by cigarette smoke extract (CSE) was studied in vitro, and small-interfering RNA (siRNA) and recombinant Klotho were employed to investigate the role of Klotho on CSE-induced autophagy. Protein levels and phosphorylation were measured by Western blot assay.

Results

CS exposure resulted in induction of autophagy in alveolar macrophages. Pretreatment of cells with Klotho attenuated CS-induced autophagy whereas knockdown of Klotho augmented CS-induced autophagy. Klotho inhibited phosphorylation of ERK, Akt, and IGF-1 in CSE-stimulated cells.

Conclusions

These data suggest that Klotho plays a critical role in the regulation of CS-induced autophagy and have important implications in understanding the mechanisms of CS-induced cell death and senescence.
Keywords:
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