PMID- 38310670
OWN - NLM
STAT- MEDLINE
DCOM- 20240226
LR  - 20240229
IS  - 1872-9142 (Electronic)
IS  - 0161-5890 (Linking)
VI  - 167
DP  - 2024 Mar
TI  - ANXA3 interference inactivates ERK/ELK1 pathway to mitigate inflammation and 
      apoptosis in sepsis-associated acute lung injury.
PG  - 25-33
LID - S0161-5890(24)00014-2 [pii]
LID - 10.1016/j.molimm.2024.01.006 [doi]
AB  - Acute lung injury (ALI) is a prevailing and deadly complication of sepsis coupled 
      with increasing incidence and fatality rate. Annexin A3 (ANXA3) has been 
      unraveled to be upregulated during sepsis. This study purposed to assess the role 
      and the mechanism of ANXA3 in sepsis-induced ALI. After the construction of mouse 
      model of sepsis, the pathological changes of mice lung tissues were estimated by 
      H&E staining. ANXA3 expression in mice lung tissues and serum was examined. The 
      degree of pulmonary edema and the levels of inflammatory factors in 
      bronchoalveolar lavage fluid (BALF) were analyzed. In lipopolysaccharide 
      (LPS)-induced mouse ALI model in vitro, CCK-8 assay measured cell viability and 
      flow cytometry analysis detected cell apoptosis. Besides, ELISA assay detected 
      the release of inflammatory cytokines. Western blot analyzed the expression of 
      proteins associated with inflammation, apoptosis and 
      extracellular-signal-regulated kinase (ERK)/ETS-like gene 1 (ELK1) signaling. 
      Results revealed that ANXA3 was overexpressed in the lung tissues and serum of 
      septic mice. Following the knockdown of ANXA3, sepsis-induced lung injury was 
      alleviated, manifested as reduced lung edema, decreased inflammatory cell 
      infiltration and inhibited cell apoptosis. Additionally, ANXA3 silence blocked 
      ERK/ELK1 signaling both in sepsis mouse models and in vitro model of ALI induced 
      by lipopolysaccharide (LPS). Moreover, the inhibitory effects of ANXA3 silencing 
      on ERK/ELK1 signaling activation, the viability damage, inflammation and 
      apoptosis in LPS-induced mouse ALI model in vitro were partially reversed by ERK 
      activator. Collectively, depletion of ANXA3 exerted suppressive effects on the 
      inflammation and apoptosis in sepsis-induced ALI through blocking ERK/ELK1 
      signaling.
CI  - Copyright (c) 2024 Elsevier Ltd. All rights reserved.
FAU - Liang, Jifang
AU  - Liang J
AD  - Intensive Care Unit, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, 
      Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, 
      Shanxi, 030032, China; Intensive Care Unit, Tongji Hospital, Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, 
      China. Electronic address: dongkekeer@163.com.
FAU - Zhang, Junkun
AU  - Zhang J
AD  - Third Hospital of Shanxi Medical University, Shanxi Bethune Hospital, Shanxi 
      Academy of Medical Sciences, Tongji Shanxi Hospital, Taiyuan, Shanxi, 030032, 
      China.
FAU - Fan, Jixiu
AU  - Fan J
AD  - General Medical Department, Shanxi Bethune Hospital, Shanxi Academy of Medical 
      Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, 
      Taiyuan, Shanxi, 030032, China; General Medical Department, Tongji Hospital, 
      Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 
      Hubei, 430030, China.
FAU - Chen, Shuxian
AU  - Chen S
AD  - Intensive Care Unit, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, 
      Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, 
      Shanxi, 030032, China; Intensive Care Unit, Tongji Hospital, Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, 
      China.
FAU - Wu, Weidong
AU  - Wu W
AD  - Intensive Care Unit, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, 
      Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, 
      Shanxi, 030032, China; Intensive Care Unit, Tongji Hospital, Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, 
      China. Electronic address: wuweidong@sxmu.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20240203
PL  - England
TA  - Mol Immunol
JT  - Molecular immunology
JID - 7905289
RN  - EC 3.1.4.43 (Annexin A3)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Elk1 protein, mouse)
SB  - IM
MH  - Animals
MH  - Mice
MH  - *Acute Lung Injury/pathology
MH  - Annexin A3/metabolism
MH  - Apoptosis
MH  - Disease Models, Animal
MH  - Extracellular Signal-Regulated MAP Kinases/metabolism
MH  - Inflammation/pathology
MH  - Lipopolysaccharides/pharmacology
MH  - Lung/metabolism
MH  - *Sepsis/metabolism
OTO - NOTNLM
OT  - ANXA3
OT  - Apoptosis
OT  - ERK/ELK1 signaling
OT  - Inflammation
OT  - Sepsis-induced acute lung injury
EDAT- 2024/02/05 00:42
MHDA- 2024/02/26 06:42
CRDT- 2024/02/04 18:01
PHST- 2023/09/04 00:00 [received]
PHST- 2023/12/21 00:00 [revised]
PHST- 2024/01/08 00:00 [accepted]
PHST- 2024/02/26 06:42 [medline]
PHST- 2024/02/05 00:42 [pubmed]
PHST- 2024/02/04 18:01 [entrez]
AID - S0161-5890(24)00014-2 [pii]
AID - 10.1016/j.molimm.2024.01.006 [doi]
PST - ppublish
SO  - Mol Immunol. 2024 Mar;167:25-33. doi: 10.1016/j.molimm.2024.01.006. Epub 2024 Feb 
      3.