PMID- 31599429
OWN - NLM
STAT- MEDLINE
DCOM- 20201006
LR  - 20201006
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 23
IP  - 18
DP  - 2019 Sep
TI  - Influence of lncRNA-MALAT1 on neuronal apoptosis in rats with cerebral infarction 
      through regulating the ERK/MAPK signaling pathway.
PG  - 8039-8048
LID - 19020 [pii]
LID - 10.26355/eurrev_201909_19020 [doi]
AB  - OBJECTIVE: To investigate the regulatory effect of long non-coding ribonucleic 
      acid (lncRNA)-metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on 
      the extracellular signal-regulated kinase/mitogen-activated protein kinase 
      (ERK/MAPK) signaling pathway, and to explore its influence on neuronal apoptosis 
      in rats with cerebral infarction. MATERIALS AND METHODS: A total of 45 adult male 
      Sprague-Dawley rats were randomly divided into sham group (n=15), model group 
      (n=15) and MALAT1 low-expression group (n=15). The model of cerebral infarction 
      was successfully established in the model group and MALAT1 low-expression group 
      via middle cerebral artery occlusion (MCAO). After 3 d, the nerve injury in each 
      group was evaluated using Zea-Longa score. Meanwhile, the area of cerebral 
      infarction in each group was detected via 2,3,5-triphenyl tetrazolium chloride 
      (TTC) staining. After the cortical tissues were separated, the expression level 
      of lncRNA-MALAT1 was detected via quantitative Polymerase Chain Reaction (qPCR). 
      The apoptotic level of neurons in each group was detected via terminal 
      deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. 
      The expression levels of inflammatory factors were detected using enzyme-linked 
      immunosorbent assay (ELISA) kits. Furthermore, the expression levels of 
      apoptosis-related proteins and ERK/MAPK signaling pathway-related proteins were 
      detected via Western blotting. RESULTS: Compared with the sham group, the 
      behavioral score and area of cerebral infarction in the model group were 
      significantly increased (p<0.01). The low expression of MALAT1 could effectively 
      reduce the behavioral score and area of cerebral infarction in the model group 
      (p<0.01). The expression level of lncRNA-MALAT1 in cortical tissues of the model 
      group was markedly higher than that of the sham group and MALAT1 low-expression 
      group (p<0.01). Compared with the sham group, the content of tumor necrosis 
      factor-alpha (TNF-alpha) and interleukin-6 (IL-6) in cortical tissues was significantly 
      increased (p<0.01). However, the content of IL-10 was remarkably decreased in the 
      model group (p<0.01). Low expressed MALAT1 could markedly reduce the content of 
      TNF-alpha and IL-6 and increase the content of IL-10 in cortical tissues (p<0.01). 
      The level of apoptosis in cortical tissues was increased in the model group when 
      compared with that of the sham group (p<0.01). Meanwhile, low expression of 
      MALAT1 could effectively reduce the apoptosis level in cortical tissues in model 
      group (p<0.01). In the model group, the expression levels of B-cell 
      lymphoma-2/Bcl-2 associated X protein (Bcl-2/Bax), p-ERK and matrix 
      metalloproteinase-2 (MMP-2) in cortical tissues were significantly declined than 
      the sham group (p<0.01). However, the protein expression level of cleaved 
      caspase-3 was markedly increased (p<0.01). Furthermore, the low expression of 
      MALAT1 could remarkably increase the expressions of Bcl-2/Bax, p-ERK and MMP-2 
      (p<0.01), as well as decrease the expression of cleaved caspase-3 (p<0.01). 
      CONCLUSIONS: LncRNA-MALAT1 may increase the release of inflammatory cytokines by 
      inhibiting the ERK/MAPK signaling pathway, thereby up-regulating the level of 
      neuronal apoptosis and aggravating the cerebral injury in rats with cerebral 
      infarction.
FAU - Shi, Y-L
AU  - Shi YL
AD  - Department of Neurology, the First Hospital of Xi'an, Xi'an, China. 
      wjc750309@163.com.
FAU - Wang, Q
AU  - Wang Q
FAU - Wei, J-C
AU  - Wei JC
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (Bax protein, rat)
RN  - 0 (Bcl2 protein, rat)
RN  - 0 (Il6 protein, rat)
RN  - 0 (Interleukin-6)
RN  - 0 (MALAT1 long noncoding RNA, rat)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (RNA, Long Noncoding)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (bcl-2-Associated X Protein)
RN  - 130068-27-8 (Interleukin-10)
RN  - EC 3.4.22.- (Casp3 protein, rat)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.24.24 (Matrix Metalloproteinase 2)
RN  - EC 3.4.24.24 (Mmp2 protein, rat)
SB  - IM
MH  - Animals
MH  - Apoptosis/*genetics
MH  - Caspase 3/metabolism
MH  - Cerebral Cortex/immunology/*metabolism/pathology
MH  - Infarction, Middle Cerebral Artery/*genetics/metabolism/pathology/physiopathology
MH  - Inflammation/immunology
MH  - Interleukin-10/immunology
MH  - Interleukin-6/immunology
MH  - *MAP Kinase Signaling System
MH  - Matrix Metalloproteinase 2/metabolism
MH  - Neurons/*metabolism/pathology
MH  - Proto-Oncogene Proteins c-bcl-2/metabolism
MH  - RNA, Long Noncoding/*genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Tumor Necrosis Factor-alpha/immunology
MH  - bcl-2-Associated X Protein/metabolism
EDAT- 2019/10/11 06:00
MHDA- 2020/10/07 06:00
CRDT- 2019/10/11 06:00
PHST- 2019/10/11 06:00 [entrez]
PHST- 2019/10/11 06:00 [pubmed]
PHST- 2020/10/07 06:00 [medline]
AID - 19020 [pii]
AID - 10.26355/eurrev_201909_19020 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2019 Sep;23(18):8039-8048. doi: 
      10.26355/eurrev_201909_19020.