PMID- 35246016
OWN - NLM
STAT- MEDLINE
DCOM- 20220408
LR  - 20220606
IS  - 2165-5987 (Electronic)
IS  - 2165-5979 (Print)
IS  - 2165-5979 (Linking)
VI  - 13
IP  - 3
DP  - 2022 Mar
TI  - Overexpression of microRNA-381-3p ameliorates hypoxia/ischemia-induced neuronal 
      damage and microglial inflammation via regulating the C-C chemokine receptor type 
      2 /nuclear transcription factor-kappa B axis.
PG  - 6839-6855
LID - 10.1080/21655979.2022.2038448 [doi]
AB  - microRNAs, as small endogenous RNAs, influence umpteen sophisticated cellular 
      biological functions regarding neurodegenerative and cerebrovascular diseases. 
      Here, we interrogated miR-381-3p's influence on BV2 activation and neurotoxicity 
      in ischemic and hypoxic environment. Oxygen-glucose deprivation (OGD) was adopted 
      to induce microglial activation and HT-22 neuron damage. Quantitative polymerase 
      chain reaction (qRT-PCR) was taken to check miR-381-3p expression in OGD-elicited 
      BV2 cells and HT-22 neurons. It transpired that miR-381-3p expression was lowered 
      in BV2 cells and HT-22 cells elicited by OGD. miR-381-3p up-regulation remarkably 
      hampered inflammatory mediator expression in BV2 cells induced by OGD and 
      weakened HT22 neuron apoptosis. In vivo, miR-381-3p expression was abated in HI 
      rats' ischemic lesions, and miR-381-3p up-regulation could ameliorate 
      inflammation and neuron apoptosis in their brain. C-C chemokine receptor type 2 
      (CCR2) was identified as the downstream target of miR-381-3p, and miR-381-3p 
      suppressed the CCR2/NF-kappaB pathway to mitigate microglial activation and 
      neurotoxicity. Therefore, we believed that miR-381-3p overexpression exerts 
      anti-inflammation and anti-apoptosis in ischemic brain injury by targeting CCR2.
FAU - Che, Yuanmei
AU  - Che Y
AD  - Department of Infection, The First Affiliated Hospital of Nanchang University, 
      Nanchang, China.
FAU - He, Jianglong
AU  - He J
AD  - Department of Infection, The First Affiliated Hospital of Nanchang University, 
      Nanchang, China.
FAU - Li, Xiaopeng
AU  - Li X
AD  - Department of Infection, The First Affiliated Hospital of Nanchang University, 
      Nanchang, China.
FAU - Wu, Daxian
AU  - Wu D
AD  - Department of Infection, The First Affiliated Hospital of Nanchang University, 
      Nanchang, China.
FAU - Zhang, Yi
AU  - Zhang Y
AD  - Department of Infection, The First Affiliated Hospital of Nanchang University, 
      Nanchang, China.
FAU - Yuan, Guicai
AU  - Yuan G
AD  - Department of Infection, The Second Affiliated Hospital of Yichun University, 
      Yichun, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Bioengineered
JT  - Bioengineered
JID - 101581063
RN  - 0 (MIRN381 microRNA, rat)
RN  - 0 (MicroRNAs)
RN  - 0 (NF-kappa B)
RN  - 0 (Receptors, Chemokine)
RN  - IY9XDZ35W2 (Glucose)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Animals
MH  - Apoptosis/genetics
MH  - Glucose/metabolism/toxicity
MH  - Hypoxia/metabolism/pathology
MH  - Inflammation/metabolism
MH  - Ischemia/metabolism/pathology
MH  - *MicroRNAs/genetics/metabolism
MH  - Microglia/metabolism
MH  - *NF-kappa B/genetics/metabolism
MH  - Neurons/metabolism
MH  - Oxygen
MH  - Rats
MH  - Receptors, Chemokine/metabolism
PMC - PMC8973660
OTO - NOTNLM
OT  - CCR2
OT  - Ischemic stroke
OT  - miR-381-3p
OT  - neuroinflammation
OT  - neuron
COIS- No potential conflict of interest was reported by the author(s).
EDAT- 2022/03/06 06:00
MHDA- 2022/04/09 06:00
PMCR- 2022/03/04
CRDT- 2022/03/05 05:24
PHST- 2022/03/05 05:24 [entrez]
PHST- 2022/03/06 06:00 [pubmed]
PHST- 2022/04/09 06:00 [medline]
PHST- 2022/03/04 00:00 [pmc-release]
AID - 2038448 [pii]
AID - 10.1080/21655979.2022.2038448 [doi]
PST - ppublish
SO  - Bioengineered. 2022 Mar;13(3):6839-6855. doi: 10.1080/21655979.2022.2038448.