PMID- 28501777
OWN - NLM
STAT- MEDLINE
DCOM- 20180319
LR  - 20181202
IS  - 1950-6007 (Electronic)
IS  - 0753-3322 (Linking)
VI  - 91
DP  - 2017 Jul
TI  - MiR-140/BDNF axis regulates normal human astrocyte proliferation and LPS-induced 
      IL-6 and TNF-alpha secretion.
PG  - 899-905
LID - S0753-3322(17)30240-8 [pii]
LID - 10.1016/j.biopha.2017.05.016 [doi]
AB  - Reactive astrocyte proliferation after spinal cord injury (SCI) contributes to 
      glial scar formation that impedes axonal regeneration. The mechanisms underlying 
      astrocyte proliferation upon injury remain partially understood. MicroRNAs 
      (miRNAs) function as a major class of post-transcriptional gene expression 
      regulators that participate in many biological processes. In this study, we 
      focused on the functional role of miR-140 in normal human astrocyte (NHA) cell 
      proliferation. Ectopic miR-140 expression significantly inhibited NHA cell 
      viability and proliferation; miR-140 inhibition exerted the opposite function. 
      Commonly, miRNAs exert functions through targeting downstream genes to inhibit 
      their expression. In the present study, brain-derived neurotrophic factor (BDNF), 
      a regulator of astrocyte proliferation and differentiation, confirmed as a direct 
      target of miR-140 in NHA. Through binding to the 3'UTR of BDNF, miR-140 inhibited 
      BDNF expression. BDNF overexpression significantly promoted NHA cell viability 
      and proliferation; the regulatory effect of miR-140/BDNF on NHA proliferation was 
      mediated by PI3K/AKT pathway. Moreover, we evaluated the functional role of 
      miR-140 in Lipopolysaccharide (LPS)-induced in vitro injury model of astroglial 
      cultures; a significantly up-regulated BDNF, interleukin (IL)-6 and tumor 
      necrosis factor (TNF)-alpha expression in response to LPS stimulation was observed. 
      After ectopic miR-140 expression, the promotive effect of LPS on BDNF, IL-6 and 
      TGF-alpha expression was partially restored. Taken together, miR-140/BDNF axis 
      regulates NHA proliferation through PI3K/AKT pathway; miR-140 could inhibit BDNF, 
      IL-6 and TGF-alpha expression in LPS-induced in vitro injury model. MiR-140/BDNF 
      might serve as a promising target in strategy against reactive astrocyte 
      proliferation after SCI.
CI  - Copyright (c) 2017. Published by Elsevier Masson SAS.
FAU - Tu, Zhiming
AU  - Tu Z
AD  - Department of Spine Surgery, The Second Xiangya Hospital of Central South 
      University, 139 Renmin Road, Changsha 410011, Hunan, China.
FAU - Li, Yawei
AU  - Li Y
AD  - Department of Spine Surgery, The Second Xiangya Hospital of Central South 
      University, 139 Renmin Road, Changsha 410011, Hunan, China.
FAU - Dai, Yuliang
AU  - Dai Y
AD  - Department of Spine Surgery, The Second Xiangya Hospital of Central South 
      University, 139 Renmin Road, Changsha 410011, Hunan, China.
FAU - Li, Lei
AU  - Li L
AD  - Department of Spine Surgery, The Second Xiangya Hospital of Central South 
      University, 139 Renmin Road, Changsha 410011, Hunan, China.
FAU - Lv, Guohua
AU  - Lv G
AD  - Department of Spine Surgery, The Second Xiangya Hospital of Central South 
      University, 139 Renmin Road, Changsha 410011, Hunan, China.
FAU - Chen, Ivan
AU  - Chen I
AD  - Department of Orthopaedic Surgery, Stanford University, 300 Pasteur Dr, Stanford, 
      CA 94305, USA.
FAU - Wang, Bing
AU  - Wang B
AD  - Department of Spine Surgery, The Second Xiangya Hospital of Central South 
      University, 139 Renmin Road, Changsha 410011, Hunan, China. Electronic address: 
      xy_wangbing@sina.com.
LA  - eng
PT  - Journal Article
DEP - 20170511
PL  - France
TA  - Biomed Pharmacother
JT  - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
JID - 8213295
RN  - 0 (3' Untranslated Regions)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (MicroRNAs)
RN  - 0 (Mirn140 microRNA, human)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 7171WSG8A2 (BDNF protein, human)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - 3' Untranslated Regions/genetics
MH  - Astrocytes/*cytology/*metabolism
MH  - Base Sequence
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Cell Proliferation/drug effects
MH  - Humans
MH  - Inflammation/pathology
MH  - Interleukin-6/*metabolism
MH  - Lipopolysaccharides/*pharmacology
MH  - MicroRNAs/*metabolism
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Protein Binding/drug effects
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Signal Transduction/drug effects
MH  - Tumor Necrosis Factor-alpha/*metabolism
OTO - NOTNLM
OT  - BDNF
OT  - Normal human astrocyte (NHA)
OT  - Proliferation
OT  - Spinal cord injury
OT  - miR-140
EDAT- 2017/05/16 06:00
MHDA- 2018/03/20 06:00
CRDT- 2017/05/15 06:00
PHST- 2017/01/16 00:00 [received]
PHST- 2017/05/03 00:00 [revised]
PHST- 2017/05/04 00:00 [accepted]
PHST- 2017/05/16 06:00 [pubmed]
PHST- 2018/03/20 06:00 [medline]
PHST- 2017/05/15 06:00 [entrez]
AID - S0753-3322(17)30240-8 [pii]
AID - 10.1016/j.biopha.2017.05.016 [doi]
PST - ppublish
SO  - Biomed Pharmacother. 2017 Jul;91:899-905. doi: 10.1016/j.biopha.2017.05.016. Epub 
      2017 May 11.