Endoplasmic reticulum stress potentiates the autophagy of alveolar macrophage to attenuate acute lung injury and airway inflammation
Authors: Bin Wang
Xiangke Cao
Jian Pei
Fumin Feng
Qingzeng Qian
Xiaoliu Dong
Ling Xue
Journal: Cell Cycle (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Endoplasmic reticulum stress; acute lung injury; airway inflammation; alveolar macrophage; autophagy
Affiliations: College of Public Health, North China University of Science and Technology, Tangshan, P. R. China., College of Life Sciences, North China University of Science and Technology, Tangshan, P. R. China., Department of Pediatrics, Affiliated Hospital of North China University of Science and Technology, Tangshan, P. R. China., Department of Neurology, Tangshan People's Hospital, Tangshan, P. R. China., Department of Neurosurgery, Tangshan Worker's Hospital, Tangshan, P. R. China.

Abstract:  Endoplasmic reticulum (ER) stress has been reported to play a role in acute lung injury (ALI), yet the in-depth mechanism remains elusive. This study aims to investigate the effect of ER stress-induced autophagy of alveolar macrophage (AM) on acute lung injury (ALI) and airway inflammation using mouse models. ALI models were induced by intranasal instillation of lipopolysaccharide (LPS). The lung weight/body weight (LW/BW) ratio and excised lung gas volume (ELGV) in each group were measured. Mouse bronchoalveolar lavage fluid (BALF) was collected for cell sorting and protein concentration determination. Expression of tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) in lung tissues and BALF was also detected. Mouse AMs were isolated to observe the autophagy. Expression of GRP78, PERK, LC3I, LC3II and Beclin1 was further determined. The results indicated that tunicamycin (TM) elevated GRP78 and PERK expression of AMs in ALI mice in a dose-dependent manner. Low dosage of TM abated LC3I expression, increased LC3II and Beclin1 expression, triggered ER stress and AM autophagy, and alleviated pathological changes of AMs in ALI mice. Also, in ALI mice, low dosage of TM attenuated goblet cell proliferation of tracheal wall, and declined LW/BW ratio, ELGV, total cells and neutrophils, protein concentrations in BALF, and IL-6 and TNF-α expression in lung tissues and BALF. Collectively, this study suggests that a low dosage of TM-induced ER stress can enhance the autophagy of AM in ALI mice models, thus attenuating the progression of ALI and airway inflammation. 

Retracted: Yes

PubPeer comments:
 Fig 4a.  Pathological changes of lung tissue in mice in each group by HE staining . ![file] Fig 4b.  Pathological changes of lung tissue in mice in each group by AB-PAS staining . First two panels, with a 180-deg flip. ![] Other four panels: ![] , 
 Retracted [17 March 2022] . -------------------------------- We, the Editors and Publisher of the journal *Cell Cycle*, have retracted the following article: Qingzeng Qian, Xiangke Cao, Bin Wang, Xiaoliu Dong, Jian Pei, Ling Xue, and Fumin Feng. Endoplasmic reticulum stress potentiates the autophagy of alveolar macrophage to attenuate acute lung injury and airway inflammation. Cell Cycle. 2020;19(5):567-576. doi: 10.1080 15384101.2020.1718851. Since publication, concerns have been raised about the integrity of the data in the article. When approached for an explanation, the authors have been unable to address all the concerns raised and have not been able to provide all their original data, or sufficient supporting information. As verifying the validity of published work is core to the integrity of the scholarly record, we are therefore retracting the article. The corresponding author listed in this publication has been informed. We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as u2018Retractedu2019. ,