PMID- 35971091
OWN - NLM
STAT- MEDLINE
DCOM- 20220817
LR  - 20220902
IS  - 1471-2261 (Electronic)
IS  - 1471-2261 (Linking)
VI  - 22
IP  - 1
DP  - 2022 Aug 15
TI  - EGR2 is a hub-gene in myocardial infarction and aggravates inflammation and 
      apoptosis in hypoxia-induced cardiomyocytes.
PG  - 373
LID - 10.1186/s12872-022-02814-3 [doi]
LID - 373
AB  - BACKGROUND: Myocardial infarction (MI) is characterized by coronary artery 
      occlusion, ischemia and hypoxia of myocardial cells, leading to irreversible 
      myocardial damage. Therefore, it is urgent to explore the potential mechanism of 
      myocardial injury during the MI process to develop effective therapies for 
      myocardial cell rescue. METHODS: We downloaded the GSE71906 dataset from GEO 
      DataSets, and the R software was used to identify the differentially expressed 
      genes (DEGs) in mouse heart tissues of MI and sham controls. Gene Ontology (GO) 
      and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment were 
      performed to understand the significantly activated signaling pathways in MI. 
      Protein-protein interaction (PPI) network was constructed to highlight the hub 
      genes in DEGs. The Western Blot, qRT-PCR and TUNEL staining were used to explore 
      the function of hub gene in hypoxia-induced cardiomyocytes in vitro. RESULTS: A 
      total of 235 DEGs were identified in GSE71906 dataset. Functional enrichment 
      analysis revealed that the upregulated genes were primarily associated with the 
      inflammatory response and apoptosis. 20 hub genes were identified in PPI network, 
      and the early growth response 2 (EGR2) was highlighted. In vitro. We confirmed 
      the EGR2 was upregulated induced by hypoxia and revealed the upregulated EGR2 
      aggravates pro-inflammation and pro-apoptotic genes expression. In addition, EGR2 
      knockout mitigates hypoxia-induced inflammation and apoptosis in cardiomyocytes. 
      CONCLUSION: The present study identified the EGR2 was a hub gene in myocardial 
      damage during MI process, the excessive EGR2 aggravates hypoxia-induced 
      myocardial damage by accelerating inflammation and apoptosis in vitro. Therefore, 
      targeting EGR2 offers a potential pharmacological strategy for myocardial cell 
      rescue in MI.
CI  - (c) 2022. The Author(s).
FAU - Bo, Zhixiang
AU  - Bo Z
AD  - Department of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital 
      of Chongqing Medical University, #76 Linjiang Road, Yuzhong District, Chongqing, 
      400010, China.
FAU - Huang, Shuwen
AU  - Huang S
AD  - Research Base of Traditional Chinese Medicine Syndrome, Fujian University of 
      Traditional Chinese Medicine, Fuzhou, 350122, China.
FAU - Li, Li
AU  - Li L
AD  - Department of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital 
      of Chongqing Medical University, #76 Linjiang Road, Yuzhong District, Chongqing, 
      400010, China.
FAU - Chen, Lin
AU  - Chen L
AD  - Department of Surgery, Wushan County Hospital of Traditional Chinese Medicine, 
      Chongqing, 400010, China.
FAU - Chen, Ping
AU  - Chen P
AD  - Department of Gastroenterology, The Fifth People's Hospital of Chongqing, 
      Chongqing, 400010, China.
FAU - Luo, Xiaoyi
AU  - Luo X
AD  - Department of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital 
      of Chongqing Medical University, #76 Linjiang Road, Yuzhong District, Chongqing, 
      400010, China.
FAU - Shi, Fang
AU  - Shi F
AD  - Department of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital 
      of Chongqing Medical University, #76 Linjiang Road, Yuzhong District, Chongqing, 
      400010, China.
FAU - Zhu, Bing
AU  - Zhu B
AD  - Department of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital 
      of Chongqing Medical University, #76 Linjiang Road, Yuzhong District, Chongqing, 
      400010, China. zhubing@cqmu.edu.cn.
FAU - Shen, Lin
AU  - Shen L
AD  - Department of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital 
      of Chongqing Medical University, #76 Linjiang Road, Yuzhong District, Chongqing, 
      400010, China. shenlin@cqmu.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20220815
PL  - England
TA  - BMC Cardiovasc Disord
JT  - BMC cardiovascular disorders
JID - 100968539
RN  - 0 (Early Growth Response Protein 2)
RN  - 0 (Egr2 protein, mouse)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Computational Biology
MH  - *Early Growth Response Protein 2/genetics/metabolism
MH  - Hypoxia/metabolism
MH  - Inflammation/metabolism
MH  - Mice
MH  - *Myocardial Infarction/genetics/metabolism
MH  - *Myocytes, Cardiac/metabolism
PMC - PMC9377070
OTO - NOTNLM
OT  - Cardiomyocytes
OT  - EGR2
OT  - Hub-gene
OT  - Hypoxia
OT  - Myocardial infarction (MI)
COIS- The authors have no relevant financial or non-financial interests to disclose.
EDAT- 2022/08/16 06:00
MHDA- 2022/08/18 06:00
PMCR- 2022/08/15
CRDT- 2022/08/15 23:32
PHST- 2022/02/22 00:00 [received]
PHST- 2022/08/06 00:00 [accepted]
PHST- 2022/08/15 23:32 [entrez]
PHST- 2022/08/16 06:00 [pubmed]
PHST- 2022/08/18 06:00 [medline]
PHST- 2022/08/15 00:00 [pmc-release]
AID - 10.1186/s12872-022-02814-3 [pii]
AID - 2814 [pii]
AID - 10.1186/s12872-022-02814-3 [doi]
PST - epublish
SO  - BMC Cardiovasc Disord. 2022 Aug 15;22(1):373. doi: 10.1186/s12872-022-02814-3.