PMID- 32016950
OWN - NLM
STAT- MEDLINE
DCOM- 20210212
LR  - 20210212
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 24
IP  - 2
DP  - 2020 Jan
TI  - MiRNA-411 attenuates inflammatory damage and apoptosis following spinal cord 
      injury.
PG  - 491-498
LID - 20022 [pii]
LID - 10.26355/eurrev_202001_20022 [doi]
AB  - OBJECTIVE: To investigate the role and regulate the target of miRNA-411 on spinal 
      cord injury. MATERIALS AND METHODS: The microglia cultured in vitro was activated 
      by lipopolysaccharide (LPS) to express the inflammatory phenotype. The 
      inflammatory response through miRNA-411 transfection in microglia was measured to 
      certain whether increased miRNA-411 suppressed interleukin-18 (IL-18) level to 
      attenuate the inflammation amplification via downregulating JNK pathway. 
      Furthermore, we established spinal cord injury (SCI) model in SD rats and further 
      explored the glial inflammatory degree and neurological recovery following 
      miRNA-411 treatment. Lastly, we estimated the hindlimbs function of SCI rats with 
      miRNA-411 administration or not within four weeks at post-SCI. RESULTS: In vitro, 
      miRNA-411 inhibited IL-18 expression and downregulated JNK pathway, along with 
      that inflammatory microglia were declined. In SCI rats, we detected the decreased 
      amounts of inflammatory microglia and reduction of the inflammatory factors after 
      miRNA-411 treatment. IL-18 and JNK pathway was also restrained resulted from 
      increased miRNA-411. In addition, apoptosis degree in injury site reduced and 
      survived axons were relatively multiple in the miRNA-411 group compared with the 
      SCI group. The Basso-Beattie-Bresnahan (BBB) locomotor scores of miRNA-411 
      treated rats were superior to those in rats with no treatment. CONCLUSIONS: 
      MiRNA-411 increase ameliorates the inflammatory microglia-induced neurological 
      lesion and promotes neural recovery by JNK pathway inhibition via negative 
      targeting IL-18 in SCI.
FAU - Sun, F
AU  - Sun F
AD  - General Hospital of Heilongjiang General Administration of Agriculture and 
      Reclamation, Haerbin, China. 13501772762@126.com.
FAU - Li, S-G
AU  - Li SG
FAU - Zhang, H-W
AU  - Zhang HW
FAU - Hua, F-W
AU  - Hua FW
FAU - Sun, G-Z
AU  - Sun GZ
FAU - Huang, Z
AU  - Huang Z
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (Inflammation Mediators)
RN  - 0 (MIRN411 microRNA, rat)
RN  - 0 (MicroRNAs)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Apoptosis/*physiology
MH  - Inflammation Mediators/antagonists & inhibitors/*metabolism
MH  - Locomotion/physiology
MH  - Male
MH  - MicroRNAs/*biosynthesis
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Spinal Cord Injuries/*metabolism/pathology/*prevention & control
EDAT- 2020/02/06 06:00
MHDA- 2021/02/13 06:00
CRDT- 2020/02/05 06:00
PHST- 2020/02/05 06:00 [entrez]
PHST- 2020/02/06 06:00 [pubmed]
PHST- 2021/02/13 06:00 [medline]
AID - 20022 [pii]
AID - 10.26355/eurrev_202001_20022 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2020 Jan;24(2):491-498. doi: 
      10.26355/eurrev_202001_20022.