PMID- 30245266
OWN - NLM
STAT- MEDLINE
DCOM- 20190501
LR  - 20190501
IS  - 1872-9142 (Electronic)
IS  - 0161-5890 (Linking)
VI  - 103
DP  - 2018 Nov
TI  - Omentin-1 protects against bleomycin-induced acute lung injury.
PG  - 96-105
LID - S0161-5890(18)30773-9 [pii]
LID - 10.1016/j.molimm.2018.09.007 [doi]
AB  - Acute lung injury (ALI) is characterized by inflammatory cell infiltration, 
      macrophage activation, and excessive pro-inflammatory cytokine production. 
      Bleomycin (BLM) is widely used to induce acute lung injury (ALI) and fibrosis in 
      murine models. Intratracheally administration of BLM leads to the early stage of 
      inflammatory response and the late stage of collagen deposition. Omentin-1 exerts 
      an anti-inflammatory role in reducing tumor necrosis factor alpha (TNF-alpha)-induced 
      cyclooxygenase-2 expression in endothelial cells and attenuating 
      lipopolysaccharide (LPS)-induced ALI. However, the role of omentin-1 in 
      BLM-induced ALI remains unclear. The aim of this study is to examine the effects 
      of omentin-1 on BLM-induced ALI. We found that omentin-1 was decreased in lungs 
      of BLM-induced ALI mice. Omentin-1 overexpression mediated by adenovirus 
      alleviated lung injury and maintained the integrity of the alveolar septa. 
      Omentin-1 overexpression also remarkably decreased the aggregation of neutrophil 
      and macrophages activation, the expression of monocyte chemotactic protein 1 
      (MCP-1), and down-regulated expression of interleukin 1beta (IL-1beta) in lungs of 
      BLM-induced ALI mice. Furthermore, we observed that omentin-1 reduced oxidative 
      stress and suppressed the activation of NF-kappaB pathway in BLM-induced ALI and 
      LPS-induced macrophages activation. Together, our findings indicated that 
      omentin-1 protected mice from BLM-induced ALI may through reducing inflammatory 
      cells recruitment and macrophages activation via alleviation of oxidative stress 
      and NF-kappaB pathway. Thus, therapeutic strategies aiming to restore omentin-1 
      levels may be valuable for the prevention of BLM-induced ALI.
CI  - Copyright (c) 2018 Elsevier Ltd. All rights reserved.
FAU - Zhou, Yan
AU  - Zhou Y
AD  - Department of Physiology, Xiangya School of Medicine, Central South University, 
      Changsha, Hunan, China.
FAU - Hao, CaiXia
AU  - Hao C
AD  - Department of Physiology, Xiangya School of Medicine, Central South University, 
      Changsha, Hunan, China.
FAU - Li, Chen
AU  - Li C
AD  - Department of Physiology, Changzhi medical college, Changzhi, Shanxi, China.
FAU - Huang, XiaoTing
AU  - Huang X
AD  - Department of Physiology, Xiangya School of Medicine, Central South University, 
      Changsha, Hunan, China.
FAU - Li, XiaoHong
AU  - Li X
AD  - Department of Physiology, Xiangya School of Medicine, Central South University, 
      Changsha, Hunan, China.
FAU - Tang, YiTing
AU  - Tang Y
AD  - Department of Physiology, Xiangya School of Medicine, Central South University, 
      Changsha, Hunan, China.
FAU - Huang, YanHong
AU  - Huang Y
AD  - Department of Physiology, Xiangya School of Medicine, Central South University, 
      Changsha, Hunan, China.
FAU - Tang, SiYuan
AU  - Tang S
AD  - Xiangya School of Nursing, Central South University, Changsha, Hunan, China.
FAU - Liu, Wei
AU  - Liu W
AD  - Xiangya School of Nursing, Central South University, Changsha, Hunan, China.
FAU - Feng, DanDan
AU  - Feng D
AD  - Department of Physiology, Xiangya School of Medicine, Central South University, 
      Changsha, Hunan, China.
FAU - Xu, JianPing
AU  - Xu J
AD  - Department of Physiology, Xiangya School of Medicine, Central South University, 
      Changsha, Hunan, China.
FAU - Yue, ShaoJie
AU  - Yue S
AD  - Department of Pediatrics, Xiangya Hospital, Central South University, Changsha, 
      Hunan, China.
FAU - Xie, Hui
AU  - Xie H
AD  - Movement System Injury and Repair Research Center, Xiangya Hospital, Central 
      South University, Changsha, Hunan, China.
FAU - Luo, ZiQiang
AU  - Luo Z
AD  - Department of Physiology, Xiangya School of Medicine, Central South University, 
      Changsha, Hunan, China. Electronic address: luoziqiang@csu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20180921
PL  - England
TA  - Mol Immunol
JT  - Molecular immunology
JID - 7905289
RN  - 0 (Cytokines)
RN  - 0 (GPI-Linked Proteins)
RN  - 0 (ITLN1 protein, human)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Lectins)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Protective Agents)
RN  - 11056-06-7 (Bleomycin)
SB  - IM
MH  - Acute Lung Injury/chemically induced/metabolism/*prevention & control
MH  - Animals
MH  - Bleomycin
MH  - Cells, Cultured
MH  - Cytokines/genetics/metabolism/*pharmacology
MH  - Female
MH  - GPI-Linked Proteins/genetics/metabolism/pharmacology
MH  - Inflammation Mediators/metabolism
MH  - Lectins/genetics/metabolism/*pharmacology
MH  - Lipopolysaccharides/pharmacology
MH  - Lung/*drug effects/metabolism/pathology
MH  - Macrophages, Peritoneal/*drug effects/metabolism
MH  - Mice, Inbred C57BL
MH  - NF-kappa B/metabolism
MH  - Protective Agents/pharmacology
MH  - Signal Transduction/drug effects
OTO - NOTNLM
OT  - Acute lung injury
OT  - Bleomycin
OT  - Inflammation
OT  - NF-kappaB pathway
OT  - Omentin-1
OT  - Oxidative stress
EDAT- 2018/09/25 06:00
MHDA- 2019/05/02 06:00
CRDT- 2018/09/25 06:00
PHST- 2018/05/06 00:00 [received]
PHST- 2018/09/05 00:00 [revised]
PHST- 2018/09/09 00:00 [accepted]
PHST- 2018/09/25 06:00 [pubmed]
PHST- 2019/05/02 06:00 [medline]
PHST- 2018/09/25 06:00 [entrez]
AID - S0161-5890(18)30773-9 [pii]
AID - 10.1016/j.molimm.2018.09.007 [doi]
PST - ppublish
SO  - Mol Immunol. 2018 Nov;103:96-105. doi: 10.1016/j.molimm.2018.09.007. Epub 2018 
      Sep 21.