PMID- 29416501
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 1662-5099 (Print)
IS  - 1662-5099 (Electronic)
IS  - 1662-5099 (Linking)
VI  - 11
DP  - 2018
TI  - Function of B-Cell CLL/Lymphoma 11B in Glial Progenitor Proliferation and 
      Oligodendrocyte Maturation.
PG  - 4
LID - 10.3389/fnmol.2018.00004 [doi]
LID - 4
AB  - B-cell CLL/lymphoma 11B (Bcl11b) - a C2H2 zinc finger transcriptional factor - is 
      known to regulate neuronal differentiation and function in the development of the 
      central nervous system (CNS). Although its expression is reduced during 
      oligodendrocyte (OLG) differentiation, its biological role in OLGs remains 
      unknown. In this study, we found that the downregulation of Bcl11b gene 
      expression in glial progenitor cells (GPCs) by lentivirus-mediated gene knockdown 
      (KD) causes a reduction in cell proliferation with inhibited expression of 
      stemness-related genes, while increasing the expression of cell cyclin regulator 
      p21. In contrast, OLG specific transcription factors (Olig1) and OLG cell 
      markers, including myelin proteolipid protein (PLP) and myelin oligodendrocyte 
      glycoprotein (MOG), were upregulated in Bcl11b-KD GPCs. Chromatin 
      immunoprecipitation (ChIP) analysis indicated that Bcl11b bound to the promoters 
      of Olig1 and PLP, suggesting that Bcl11b could act as a repressor for Olig1 and 
      PLP, similar to its action on p21. An increase in the number of GC(+)- or PLP(+)- 
      OLGs derived from Bcl11b-KD GPCs or OLG precursor cells was also observed. 
      Moreover, myelin basic protein (MBP) expression in OLGs derived from Bcl11b-KD 
      GPCs was enhanced in hippocampal neuron co-cultures and in cerebellar brain-slice 
      cultures. The in vivo study using a lysolecithin-induced demyelinating animal 
      model also indicated that larger amounts of MBP(+)-OLGs and PLP(+)-OLGs derived 
      from implanted Bcl11b-KD GPCs were present at the lesioned site of the white 
      matter than in the scramble group. Taken together, our results provide insight 
      into the functional role of Bcl11b in the negative regulation of GPC 
      differentiation through the repression of OLG differentiation-associated genes.
FAU - Wang, Chih-Yen
AU  - Wang CY
AD  - Institute of Life Sciences, College of Bioscience and Biotechnology, National 
      Cheng Kung University, Tainan, Taiwan.
FAU - Sun, Yuan-Ting
AU  - Sun YT
AD  - Department of Neurology, National Cheng Kung University Hospital, College of 
      Medicine, National Cheng Kung University, Tainan, Taiwan.
FAU - Fang, Kuan-Min
AU  - Fang KM
AD  - Institute of Life Sciences, College of Bioscience and Biotechnology, National 
      Cheng Kung University, Tainan, Taiwan.
FAU - Ho, Chia-Hsin
AU  - Ho CH
AD  - Institute of Life Sciences, College of Bioscience and Biotechnology, National 
      Cheng Kung University, Tainan, Taiwan.
FAU - Yang, Chung-Shi
AU  - Yang CS
AD  - Institute of Biomedical Engineering and Nanomedicine, National Health Research 
      Institutes, Zhunan, Taiwan.
FAU - Tzeng, Shun-Fen
AU  - Tzeng SF
AD  - Institute of Life Sciences, College of Bioscience and Biotechnology, National 
      Cheng Kung University, Tainan, Taiwan.
LA  - eng
PT  - Journal Article
DEP - 20180124
PL  - Switzerland
TA  - Front Mol Neurosci
JT  - Frontiers in molecular neuroscience
JID - 101477914
PMC - PMC5787563
OTO - NOTNLM
OT  - Bcl11b
OT  - differentiation and proliferation
OT  - glia
OT  - glial progenitors
OT  - oligodendrocytes
EDAT- 2018/02/09 06:00
MHDA- 2018/02/09 06:01
PMCR- 2018/01/01
CRDT- 2018/02/09 06:00
PHST- 2017/10/09 00:00 [received]
PHST- 2018/01/03 00:00 [accepted]
PHST- 2018/02/09 06:00 [entrez]
PHST- 2018/02/09 06:00 [pubmed]
PHST- 2018/02/09 06:01 [medline]
PHST- 2018/01/01 00:00 [pmc-release]
AID - 10.3389/fnmol.2018.00004 [doi]
PST - epublish
SO  - Front Mol Neurosci. 2018 Jan 24;11:4. doi: 10.3389/fnmol.2018.00004. eCollection 
      2018.