PMID- 32491927
OWN - NLM
STAT- MEDLINE
DCOM- 20201022
LR  - 20201022
IS  - 1522-1563 (Electronic)
IS  - 0363-6143 (Linking)
VI  - 319
IP  - 2
DP  - 2020 Aug 1
TI  - Overexpressed microRNA-539-5p inhibits inflammatory response of neurons to impede 
      the progression of cerebral ischemic injury by histone deacetylase 1.
PG  - C381-C391
LID - 10.1152/ajpcell.00576.2019 [doi]
AB  - Several microRNAs (miRNAs or miRs) regulate cerebral ischemic injury outcomes; 
      however, little is known about the role of miR-539-5p during cerebral ischemic 
      injury or the postischemic state. Cerebral ischemic injury was modeled in vitro 
      by exposing human cortical neurons to oxygen-glucose deprivation (OGD) and in 
      vivo by occluding the middle cerebral artery (MCAO) in a rat model. The effects 
      of miR-539-5p, histone deacetylase 1 (HDAC1), and early growth response 2 (EGR2) 
      on cerebral ischemia were investigated using gain- and loss-of-function 
      experiments. We identified changes in miR-539-5p, HDAC1, EGR2, and phosphorylated 
      c-Jun NH(2)-terminal kinase (JNK). The interaction among miR-539-5p, HDAC1, and 
      EGR2 was determined by dual luciferase reporter gene assay, chromatin 
      immunoprecipitation, and coimmunoprecipitation. We also investigated the effects 
      on cell viability and apoptosis and changes in inflammatory cytokine expression 
      and spatial memory on MCAO rats. miR-539-5p and EGR2 were poorly expressed, while 
      HDAC1 was highly expressed in OGD-treated HCN-2 cells. miR-539-5p targeted HDAC1, 
      while HDAC1 prevented acetylation of EGR2 resulting in its downregulation and 
      subsequent activation of the JNK pathway. Overexpression of miR-539-5p or EGR2 or 
      silencing HDAC1 improved viability and reduced apoptosis of OGD-treated HCN-2 
      cells in vitro. Furthermore, overexpression of miR-539-5p improved spatial 
      memory, while decreasing cell apoptosis and inflammation in MCAO rats. 
      Collectively, these data suggest that miR-539-5p targets HDAC1 to upregulate 
      EGR2, thus blocking the JNK signaling pathway, by which cerebral ischemic injury 
      is alleviated.
FAU - Xue, Hang
AU  - Xue H
AD  - Department of Neurotraumatic Surgery, The First Hospital of Jilin University, 
      Changchun, People's Republic of China.
FAU - Liu, Jianpeng
AU  - Liu J
AD  - Department of Neurosurgery, Yuncheng Central Hospital, Yuncheng, People's 
      Republic of China.
FAU - Shi, Lin
AU  - Shi L
AD  - Department of Neurotraumatic Surgery, The First Hospital of Jilin University, 
      Changchun, People's Republic of China.
FAU - Yang, Hongfa
AU  - Yang H
AUID- ORCID: 0000-0002-8409-4889
AD  - Department of Neurotraumatic Surgery, The First Hospital of Jilin University, 
      Changchun, People's Republic of China.
LA  - eng
PT  - Journal Article
PT  - Retracted Publication
DEP - 20200603
PL  - United States
TA  - Am J Physiol Cell Physiol
JT  - American journal of physiology. Cell physiology
JID - 100901225
RN  - 0 (Cytokines)
RN  - 0 (Early Growth Response Protein 2)
RN  - 0 (Egr2 protein, rat)
RN  - 0 (MIRN539 microRNA, human)
RN  - 0 (MIRN539 microRNA, rat)
RN  - 0 (MicroRNAs)
RN  - EC 3.5.1.98 (HDAC1 protein, human)
RN  - EC 3.5.1.98 (Hdac1 protein, rat)
RN  - EC 3.5.1.98 (Histone Deacetylase 1)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
RIN - Am J Physiol Cell Physiol. 2020 Nov 1;319(5):C945. PMID: 33166174
MH  - Animals
MH  - Apoptosis/genetics
MH  - Brain Ischemia/*genetics/pathology
MH  - Cytokines/metabolism
MH  - Disease Progression
MH  - Early Growth Response Protein 2/genetics
MH  - Gene Expression Regulation/genetics
MH  - Glucose/metabolism
MH  - Histone Deacetylase 1/*genetics
MH  - Humans
MH  - Inflammation/genetics
MH  - MicroRNAs/*genetics
MH  - Middle Cerebral Artery/injuries/pathology
MH  - Neurons/metabolism/pathology
MH  - Rats
OTO - NOTNLM
OT  - c-Jun NH2-terminal kinase pathway
OT  - cerebral ischemic injury
OT  - early growth response 2
OT  - histone deacetylase 1
OT  - inflammation
OT  - microRNA-539-5p
EDAT- 2020/06/04 06:00
MHDA- 2020/10/23 06:00
CRDT- 2020/06/04 06:00
PHST- 2020/06/04 06:00 [pubmed]
PHST- 2020/10/23 06:00 [medline]
PHST- 2020/06/04 06:00 [entrez]
AID - 10.1152/ajpcell.00576.2019 [doi]
PST - ppublish
SO  - Am J Physiol Cell Physiol. 2020 Aug 1;319(2):C381-C391. doi: 
      10.1152/ajpcell.00576.2019. Epub 2020 Jun 3.