PMID- 32096189
OWN - NLM
STAT- MEDLINE
DCOM- 20210211
LR  - 20210211
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 24
IP  - 3
DP  - 2020 Feb
TI  - Influence of miR-155 on behaviors of depression mice through regulating 
      Wnt/beta-catenin signaling pathway.
PG  - 1398-1407
LID - 20197 [pii]
LID - 10.26355/eurrev_202002_20197 [doi]
AB  - OBJECTIVE: To study the influence of micro ribonucleic acid (miR)-155 on 
      depression-like behaviors of depression mice, and to explore the role of 
      Wnt/b-catenin signaling pathway in behavioral regulation of depression mice. 
      MATERIALS AND METHODS: The mouse model of depression was established via chronic 
      unpredictable mild stress (CUMS). All mice were randomly divided into control 
      group (n=12), model group (n=12), and fluoxetine group (n=12). The expression 
      level of miR-155 in the hippocampus of mice in each group was detected via 
      quantitative Polymerase Chain Reaction (qPCR). The changes in the behaviors of 
      mice in each group were evaluated via behavioral experiments. The apoptosis level 
      in the hippocampus of mice in each group was detected via terminal 
      deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. 
      Moreover, the content of inflammatory factors in the hippocampus of mice in each 
      group was detected using the enzyme-linked immunosorbent assay (ELISA) kits. The 
      expression levels of Wnt/b-catenin signaling pathway-related proteins in each 
      group were detected via Western blotting. RESULTS: The expression level of 
      miR-155 in the hippocampus was significantly higher in model group than that in 
      control group (p<0.01). Meanwhile, the expression level of miR-155 was 
      significantly lower in fluoxetine group than that in model group (p<0.01). There 
      were no statistically significant differences in the crossing score and rearing 
      score in the open field test among groups (p>0.05). Compared with those in 
      control group, the immobility time in tail suspension test and forced swimming 
      test were significantly increased (p<0.01), while the sucrose preference degree 
      significantly declined (p<0.01) in model group. Fluoxetine could significantly 
      reduce the immobility time in tail suspension test and forced swimming test 
      (p<0.01) and increase the sucrose preference degree (p<0.01) in model group. The 
      number of TUNEL-positive cells in the hippocampus of mice in model group was 
      significantly larger than that in control group (p<0.01). Fluoxetine could 
      effectively reduce the number of TUNEL-positive cells in the hippocampus 
      (p<0.01). Compared with those in control group, the content of tumor necrosis 
      factor-alpha (TNF-a), interleukin-1b (IL-1b), and IL-6 in the hippocampus was 
      significantly increased (p<0.01), while the content of IL-10 was significantly 
      decreased (p<0.01) in model group. Fluoxetine could effectively reduce the 
      content of TNF-a, IL-1b, and IL-6 (p<0.01) and increase the content of IL-10 
      (p<0.01). Besides, in model group, the expression levels of dishevelled-1 (DVL-1) 
      and b-catenin in hippocampus remarkably declined (p<0.01), while the expression 
      levels of glycogen synthase kinase-3b (GSK-3b) and adenomatous polyposis coli 
      (APC) were remarkably increased (p<0.01) compared with those in control group. 
      Fluoxetine could effectively lower the expressions of GSK-3b and APC in the 
      hippocampus (p<0.01) and increase the expressions of DVL-1 and b-catenin (p<0.01) 
      in model group. CONCLUSIONS: MiR-155 is involved in regulating the 
      depression-like behaviors of depression mice through promoting the release of 
      inflammatory factors and the apoptosis of hippocampal neurons. Its mechanism may 
      be related to the inhibition of the Wnt/b-catenin signaling pathway.
FAU - Dai, J
AU  - Dai J
AD  - Department of Psychiatry, The First Affiliated Hospital of Jinan University, 
      Guangzhou, China. fjptdj@163.com.
FAU - Pan, J-Y
AU  - Pan JY
FAU - Liao, N
AU  - Liao N
FAU - Shi, J
AU  - Shi J
FAU - Zeng, Q
AU  - Zeng Q
FAU - Huang, L
AU  - Huang L
FAU - Chen, L-P
AU  - Chen LP
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 (Antidepressive Agents, Second-Generation)
RN  - 0 (CTNNB1 protein, mouse)
RN  - 0 (MicroRNAs)
RN  - 0 (Mirn155 microRNA, mouse)
RN  - 0 (beta Catenin)
RN  - 01K63SUP8D (Fluoxetine)
SB  - IM
MH  - Animals
MH  - Antidepressive Agents, Second-Generation/pharmacology/therapeutic use
MH  - Depression/drug therapy/*metabolism/psychology
MH  - Fluoxetine/pharmacology/therapeutic use
MH  - Hippocampus/drug effects/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - MicroRNAs/*biosynthesis
MH  - Random Allocation
MH  - Stress, Psychological/drug therapy/metabolism/psychology
MH  - Wnt Signaling Pathway/drug effects/*physiology
MH  - beta Catenin/antagonists & inhibitors/*metabolism
EDAT- 2020/02/26 06:00
MHDA- 2021/02/12 06:00
CRDT- 2020/02/26 06:00
PHST- 2020/02/26 06:00 [entrez]
PHST- 2020/02/26 06:00 [pubmed]
PHST- 2021/02/12 06:00 [medline]
AID - 20197 [pii]
AID - 10.26355/eurrev_202002_20197 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2020 Feb;24(3):1398-1407. doi: 
      10.26355/eurrev_202002_20197.