PMID- 36334381
OWN - NLM
STAT- MEDLINE
DCOM- 20221213
LR  - 20230322
IS  - 2213-2317 (Electronic)
IS  - 2213-2317 (Linking)
VI  - 58
DP  - 2022 Dec
TI  - Macrophage Sprouty4 deficiency diminishes sepsis-induced acute lung injury in 
      mice.
PG  - 102513
LID - S2213-2317(22)00285-3 [pii]
LID - 10.1016/j.redox.2022.102513 [doi]
LID - 102513
AB  - OBJECTIVE: Inflammation and oxidative stress play critical roles in 
      sepsis-induced acute lung injury (ALI). Sprout4 (Spry4) is involved in regulating 
      inflammation and tissue injury; however, its role and mechanism in sepsis-induced 
      ALI remain elusive. METHODS: Macrophage-specific Spry4 knockout (Spry4(MKO)), 
      transgenic (Spry4(MTG)) mice and matched control littermates were generated and 
      exposed to cecum ligation and puncture (CLP) surgery to establish bacterial 
      sepsis-induced ALI. Bone marrow-derived macrophages (BMDMs) from Spry4(MKO) or 
      Spry4(MTG) mice were isolated and subjected to lipopolysaccharide (LPS) 
      stimulation to further validate the role of Spry4 in vitro. To verify the 
      necessity of AMP-activated protein kinase (AMPK), Spry4 and AMPK double knockout 
      mice and compound C were used in vivo and in vitro. BMDMs were treated with 
      STO-609 to inhibit calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2). 
      RESULTS: We found that macrophage Spry4 was increased in CLP mice and positively 
      correlated with sepsis-induced ALI. Macrophage Spry4 deficiency prevented, while 
      macrophage Spry4 overexpression exacerbated sepsis-induced inflammation, 
      oxidative stress and ALI in mice and BMDMs. Mechanistic studies revealed that 
      macrophage Spry4 deficiency alleviated sepsis-induced ALI through activating 
      CaMKK2/AMPK pathway. CONCLUSION: Our study identify macrophage Spry4 as a 
      promising predictive and therapeutic target of sepsis-induced ALI.
CI  - Copyright (c) 2022 The Authors. Published by Elsevier B.V. All rights reserved.
FAU - Chen, Rong
AU  - Chen R
AD  - Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, 430060, 
      China.
FAU - Cao, Chen
AU  - Cao C
AD  - Medical Center, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
FAU - Liu, Huimin
AU  - Liu H
AD  - Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, 430060, 
      China.
FAU - Jiang, Wanli
AU  - Jiang W
AD  - Department of Thoracic Surgery, Renmin Hospital of Wuhan University, Wuhan, 
      430060, China.
FAU - Pan, Rui
AU  - Pan R
AD  - Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, 430060, 
      China.
FAU - He, He
AU  - He H
AD  - Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, 430060, 
      China.
FAU - Ding, Ke
AU  - Ding K
AD  - Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, 430060, 
      China.
FAU - Meng, Qingtao
AU  - Meng Q
AD  - Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, 430060, 
      China. Electronic address: mengqingtao2018@126.com.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20221022
PL  - Netherlands
TA  - Redox Biol
JT  - Redox biology
JID - 101605639
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Spry4 protein, mouse)
RN  - 0 (Nerve Tissue Proteins)
SB  - IM
EIN - Redox Biol. 2023 Jun;62:102667. PMID: 36948902
MH  - Animals
MH  - Mice
MH  - *Acute Lung Injury/genetics/chemically induced
MH  - AMP-Activated Protein Kinases
MH  - Inflammation
MH  - Lipopolysaccharides/adverse effects
MH  - Lung/metabolism
MH  - *Macrophages/metabolism
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - *Sepsis/complications/genetics
MH  - *Nerve Tissue Proteins/genetics
PMC - PMC9637958
OTO - NOTNLM
OT  - AMPK
OT  - Acute lung injury
OT  - Inflammation
OT  - Oxidative stress
OT  - Sprouty4
COIS- Declaration of competing interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2022/11/06 06:00
MHDA- 2022/12/15 06:00
PMCR- 2022/10/22
CRDT- 2022/11/05 19:11
PHST- 2022/09/12 00:00 [received]
PHST- 2022/10/10 00:00 [revised]
PHST- 2022/10/15 00:00 [accepted]
PHST- 2022/11/06 06:00 [pubmed]
PHST- 2022/12/15 06:00 [medline]
PHST- 2022/11/05 19:11 [entrez]
PHST- 2022/10/22 00:00 [pmc-release]
AID - S2213-2317(22)00285-3 [pii]
AID - 102513 [pii]
AID - 10.1016/j.redox.2022.102513 [doi]
PST - ppublish
SO  - Redox Biol. 2022 Dec;58:102513. doi: 10.1016/j.redox.2022.102513. Epub 2022 Oct 
      22.