PMID- 30841460
OWN - NLM
STAT- MEDLINE
DCOM- 20190621
LR  - 20230621
IS  - 1950-6007 (Electronic)
IS  - 0753-3322 (Linking)
VI  - 111
DP  - 2019 Mar
TI  - Repression of long non-coding RNA MEG3 restores nerve growth and alleviates 
      neurological impairment after cerebral ischemia-reperfusion injury in a rat 
      model.
PG  - 1447-1457
LID - S0753-3322(18)34567-0 [pii]
LID - 10.1016/j.biopha.2018.12.067 [doi]
AB  - OBJECTIVE: This study was performed to investigate effect of long non-coding RNA 
      (lncRNA) MEG3 on nerve growth and neurological impairment in a rat model after 
      cerebral ischemia-reperfusion injury (IRI) through the Wnt/beta-catenin signaling 
      pathway. METHODS: Rat models of middle cerebral artery occlusion (MCAO) were 
      established to stimulate an environment of cerebral IRI. The modeled rats were 
      subjected to negative control (NC), MEG3, si-MEG3, classical Wnt pathway 
      inhibitor DKK1 or classical Wnt pathway activator LiCl to validate the effect of 
      MEG3 on neurological impairment and nerve growth. Neurological deficit scoring, 
      fault-foot test and balance beam test were performed to assess neurological 
      impairment. TTC staining, dry-wet weight method and Evan's blue (EB) staining 
      were employed to determine infarct area, water content of brain tissues and 
      blood-brain barrier (BBB) permeability, respectively. Neuronal apoptosis and 
      necrosis were observed by TUNEL staining and Fluoro-Jade C staining. ELISA was 
      adopted to identify levels of nerve growth factors to identify neurogenesis 
      conditions, including brain derived neurotrophic factor (BDNF), nerve growth 
      factor (NGF) and basic fibroblast growth factor (bFGF). Nissl staining was used 
      to detect the survival of neurons in brain tissues of rats. Western blot analysis 
      was used to detect the expression of key proteins in Wnt/beta-catenin signaling 
      pathway in brain tissues. RESULTS: High expression of MEG3 was identified in rat 
      models of MACAO, the brain tissues of which manifested obvious neurological 
      impairment, increased infarct area, water content, BBB permeability, accelerated 
      neuronal apoptosis and necrosis, increased surviving neurons, upregulated 
      expression of key proteins in Wnt/beta-catenin signaling pathway and elevated levels 
      of BDNF, NGF and bFGF. With the treatment of si-MEG3, the MEG3 expression was 
      reduced; whereby, modeled rats showed ameliorated neurological impairment, 
      reduced infarct area, water content, BBB permeability, neuronal apoptosis and 
      necrosis and significantly enhanced neurogenesis. The treatment of MEG3 exhibited 
      an opposite trend. After treatment with DKK1, the effect of si-MEG3 was reversed. 
      After treatment with LiCl, the effect of MEG3 was reversed. CONCLUSION: Based on 
      the findings of this study, down-regulation of lncRNA MEG3 expression enhanced 
      nerve growth and alleviated neurological impairment of rats after cerebral IRI 
      through the activation of the Wnt/beta-catenin signaling pathway.
CI  - Copyright (c) 2018. Published by Elsevier Masson SAS.
FAU - You, Dong
AU  - You D
AD  - Department of Thoracic Surgery, The First Hospital of Jilin University, 
      Changchun, 130021, China.
FAU - You, Hong
AU  - You H
AD  - Department of Neurosurgery, The First Hospital of Jilin University, Changchun, 
      130021, China. Electronic address: yh2997@163.com.
LA  - eng
PT  - Journal Article
PT  - Retracted Publication
DEP - 20190123
PL  - France
TA  - Biomed Pharmacother
JT  - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
JID - 8213295
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (MEG3 non-coding RNA, mouse)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (RNA, Long Noncoding)
RN  - 103107-01-3 (Fibroblast Growth Factor 2)
RN  - 9061-61-4 (Nerve Growth Factor)
SB  - IM
ECI - Biomed Pharmacother. 2022 Nov;155:113856. PMID: 36271536
RIN - Biomed Pharmacother. 2023 Aug;164:114726. PMID: 37087338
MH  - Animals
MH  - Apoptosis/genetics
MH  - Blood-Brain Barrier/physiology
MH  - Brain/physiology
MH  - Brain Ischemia/*genetics
MH  - Brain-Derived Neurotrophic Factor/genetics
MH  - Disease Models, Animal
MH  - Down-Regulation/genetics
MH  - Fibroblast Growth Factor 2/genetics
MH  - Infarction, Middle Cerebral Artery/genetics
MH  - Male
MH  - Nerve Growth Factor/genetics
MH  - Neurogenesis/*genetics
MH  - Neurons/*physiology
MH  - Neuroprotective Agents
MH  - RNA, Long Noncoding/*genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reperfusion Injury/*genetics
MH  - Up-Regulation/genetics
MH  - Wnt Signaling Pathway/genetics
OTO - NOTNLM
OT  - Balance beam test
OT  - Cerebral ischemia-reperfusion injury
OT  - Fault-foot test
OT  - MEG3
OT  - Neurological impairment
OT  - Neuronal apoptosis
OT  - Neuronal necrosis
OT  - Wnt/beta-catenin signaling pathway
EDAT- 2019/03/08 06:00
MHDA- 2019/06/22 06:00
CRDT- 2019/03/08 06:00
PHST- 2018/07/04 00:00 [received]
PHST- 2018/12/08 00:00 [revised]
PHST- 2018/12/14 00:00 [accepted]
PHST- 2019/03/08 06:00 [entrez]
PHST- 2019/03/08 06:00 [pubmed]
PHST- 2019/06/22 06:00 [medline]
AID - S0753-3322(18)34567-0 [pii]
AID - 10.1016/j.biopha.2018.12.067 [doi]
PST - ppublish
SO  - Biomed Pharmacother. 2019 Mar;111:1447-1457. doi: 10.1016/j.biopha.2018.12.067. 
      Epub 2019 Jan 23.