PMID- 28790168
OWN - NLM
STAT- MEDLINE
DCOM- 20180608
LR  - 20181113
IS  - 1573-4935 (Electronic)
IS  - 0144-8463 (Print)
IS  - 0144-8463 (Linking)
VI  - 37
IP  - 4
DP  - 2017 Aug 31
TI  - MicroRNA-211/BDNF axis regulates LPS-induced proliferation of normal human 
      astrocyte through PI3K/AKT pathway.
LID - BSR20170755 [pii]
LID - 10.1042/BSR20170755 [doi]
AB  - Spinal cord injury (SCI) makes a major contribution to disability and deaths 
      worldwide. Reactive astrogliosis, a typical feature after SCI, which undergoes 
      varying molecular and morphological changes, is ubiquitous but poorly understood. 
      Reactive astrogliosis contributes to glial scar formation that impedes axonal 
      regeneration. Brain-derived neurotrophic factor (BDNF), a well-established 
      neurotrophic factor, exerts neuroprotective and growth-promoting effects on a 
      variety of neuronal populations after injury. In the present study, by using 
      LPS-induced in vitro injury model of astroglial cultures, we observed a high 
      expression of interleukin (IL)-6, IL-1beta, and BDNF in LPS-stimulated normal human 
      astrocytes (NHAs). BDNF significantly promoted NHA proliferation. Further, online 
      tools were employed to screen the candidate miRNAs which might directly target 
      BDNF to inhibit its expression. Amongst the candidate miRNAs, miR-211 expression 
      was down-regulated by LPS stimulation in a dose-dependent manner. Through direct 
      targetting, miR-211 inhibited BDNF expression. Ectopic miR-211 expression 
      significantly suppressed NHA proliferation, as well as LPS-induced activation of 
      PI3K/Akt pathway. In contrast, inhibition of miR-211 expression significantly 
      promoted NHA proliferation and LPS-induced activation of PI3K/Akt pathway. Taken 
      together, miR-211/BDNF axis regulates LPS-induced NHA proliferation through 
      PI3K/AKT pathway; miR-211/BDNF might serve as a promising target in the strategy 
      against reactive astrocyte proliferation after SCI.
CI  - (c) 2017 The Author(s).
FAU - Zhang, Kexiang
AU  - Zhang K
AD  - Department of Orthopedics, The Third Xiangya Hospital, Central South University, 
      Changsha 410013, China.
FAU - Wu, Song
AU  - Wu S
AD  - Department of Orthopedics, The Third Xiangya Hospital, Central South University, 
      Changsha 410013, China.
FAU - Li, Zhiyue
AU  - Li Z
AD  - Department of Orthopedics, The Third Xiangya Hospital, Central South University, 
      Changsha 410013, China.
FAU - Zhou, Jiahui
AU  - Zhou J
AD  - Department of Orthopedics, The Third Xiangya Hospital, Central South University, 
      Changsha 410013, China zjh5518@sina.com.
LA  - eng
PT  - Journal Article
DEP - 20170821
PL  - England
TA  - Biosci Rep
JT  - Bioscience reports
JID - 8102797
RN  - 0 (3' Untranslated Regions)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (MIRN211 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 7171WSG8A2 (BDNF protein, human)
RN  - EC 2.7.1.137 (Phosphatidylinositol 3-Kinase)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - 3' Untranslated Regions
MH  - Astrocytes/*metabolism
MH  - Brain-Derived Neurotrophic Factor/genetics/*metabolism
MH  - Cell Proliferation/*drug effects
MH  - Cells, Cultured
MH  - Cicatrix/metabolism
MH  - Dose-Response Relationship, Drug
MH  - Down-Regulation
MH  - HEK293 Cells
MH  - Humans
MH  - Lipopolysaccharides/*pharmacology
MH  - MicroRNAs/genetics/*metabolism
MH  - Phosphatidylinositol 3-Kinase/*metabolism
MH  - Proto-Oncogene Proteins c-akt/*metabolism
MH  - Spinal Cord Injuries/chemically induced
PMC - PMC5563540
OTO - NOTNLM
OT  - Brain-derived Neurotrophic Factor (BDNF)
OT  - miR-211
OT  - normal human astrocyte (NHA)
OT  - proliferation
OT  - spinal cord injury (SCI)
COIS- The authors declare that there are no competing interests associated with the 
      manuscript.
EDAT- 2017/08/10 06:00
MHDA- 2018/06/09 06:00
PMCR- 2017/08/21
CRDT- 2017/08/10 06:00
PHST- 2017/05/05 00:00 [received]
PHST- 2017/07/20 00:00 [revised]
PHST- 2017/08/08 00:00 [accepted]
PHST- 2017/08/10 06:00 [pubmed]
PHST- 2018/06/09 06:00 [medline]
PHST- 2017/08/10 06:00 [entrez]
PHST- 2017/08/21 00:00 [pmc-release]
AID - BSR20170755 [pii]
AID - 10.1042/BSR20170755 [doi]
PST - epublish
SO  - Biosci Rep. 2017 Aug 21;37(4):BSR20170755. doi: 10.1042/BSR20170755. Print 2017 
      Aug 31.