PMID- 31875620
OWN - NLM
STAT- MEDLINE
DCOM- 20200219
LR  - 20211204
IS  - 1349-3299 (Electronic)
IS  - 1349-2365 (Linking)
VI  - 61
IP  - 1
DP  - 2020 Jan 31
TI  - Exercise Preconditioning Protects against Acute Cardiac Injury Induced by 
      Lipopolysaccharide Through General Control Nonderepressible 2 Kinase.
PG  - 138-144
LID - 10.1536/ihj.19-307 [doi]
AB  - Exercise preconditioning may protect against cardiac injury induced by 
      lipopolysaccharide (LPS), but the mechanism is unresolved. The aim of this study 
      is to explore whether the general control nonderepressible 2 (GCN2) kinase gene 
      is associated with the protective effect of exercise preconditioning. 
      Eight-week-old male C57BL/6J (n = 40) and GCN2 knockout (KO) (n = 40) mice were 
      divided into four groups: control, LPS (L), exercise preconditioning (E), and 
      exercise preconditioning LPS (EL). Mice in the exercise groups performed exercise 
      for eight weeks. After exercise, all mice were given an equal volume of LPS or 
      saline (10 mug/g). We measured the cardiac function using echocardiography and 
      then collected heart tissue. Exercise preconditioning improved cardiac 
      inflammation (interleukin-6, tumor necrosis factor alpha) and cardiac dysfunction 
      (ejection fraction, fraction shortening) in C57 mice induced by LPS and also 
      decreased the expression levels of GCN2, phosphorylation of eukaryotic 
      translation initiation factor 2alpha (p-eIF2alpha), and activating transcription factor 4 
      (ATF4). Moreover, GCN2 KO decreased inflammation and cardiac dysfunction induced 
      by LPS in sedentary mice. The inflammation and cardiac dysfunction in the GCN2 KO 
      EL group were lower than in the C57 EL group, and the expression of GCN2, 
      p-eIF2alpha, and ATF4 in the GCN2 KO EL group was lower than in the C57 EL group. 
      Exercise preconditioning alleviated cardiac injury induced by LPS. GCN2 KO also 
      improved cardiac injury. Exercise preconditioning promoted the effect of GCN2 KO 
      in alleviating cardiac injury, and the GCN2 and eIF2alpha/ATF4 pathways play an 
      important role in the process.
FAU - Sun, Zhong-Guang
AU  - Sun ZG
AD  - Department of Exercise Rehabilitation, Shanghai University of Sport.
FAU - Lu, Guo
AU  - Lu G
AD  - Department of Exercise Rehabilitation, Shanghai University of Sport.
FAU - Zhao, Lin-Lin
AU  - Zhao LL
AD  - Department of Exercise Rehabilitation, Shanghai University of Sport.
FAU - Zhang, Li-Zhen
AU  - Zhang LZ
AD  - Department of Exercise Rehabilitation, Shanghai University of Sport.
FAU - Li, Ai
AU  - Li A
AD  - Department of Exercise Rehabilitation, Shanghai University of Sport.
FAU - Jing, Jing
AU  - Jing J
AD  - Department of Exercise Rehabilitation, Shanghai University of Sport.
FAU - Xu, Xin
AU  - Xu X
AD  - Department of Exercise Rehabilitation, Shanghai University of Sport.
LA  - eng
PT  - Journal Article
DEP - 20191226
PL  - Japan
TA  - Int Heart J
JT  - International heart journal
JID - 101244240
RN  - 0 (Atf4 protein, mouse)
RN  - 0 (Eukaryotic Initiation Factor-2)
RN  - 0 (Lipopolysaccharides)
RN  - 145891-90-3 (Activating Transcription Factor 4)
RN  - EC 2.7.11.1 (Eif2ak4 protein, mouse)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
SB  - IM
MH  - Activating Transcription Factor 4/metabolism
MH  - Animals
MH  - Disease Models, Animal
MH  - Echocardiography
MH  - Eukaryotic Initiation Factor-2/metabolism
MH  - Gene Knockout Techniques
MH  - Heart Injuries/chemically induced/diagnosis/metabolism/*prevention & control
MH  - Lipopolysaccharides/*adverse effects
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Phosphorylation
MH  - Physical Conditioning, Animal/*methods
MH  - Protein Serine-Threonine Kinases/*genetics/metabolism
OTO - NOTNLM
OT  - Eukaryotic initiation factor 2alpha
OT  - Inflammation
EDAT- 2019/12/26 06:00
MHDA- 2020/02/20 06:00
CRDT- 2019/12/26 06:00
PHST- 2019/12/26 06:00 [pubmed]
PHST- 2020/02/20 06:00 [medline]
PHST- 2019/12/26 06:00 [entrez]
AID - 10.1536/ihj.19-307 [doi]
PST - ppublish
SO  - Int Heart J. 2020 Jan 31;61(1):138-144. doi: 10.1536/ihj.19-307. Epub 2019 Dec 
      26.