PMID- 27291422
OWN - NLM
STAT- MEDLINE
DCOM- 20180426
LR  - 20181113
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 6
DP  - 2016 Jun 13
TI  - Inflammation-induced reversible switch of the neuron-specific enolase promoter 
      from Purkinje neurons to Bergmann glia.
PG  - 27758
LID - 10.1038/srep27758 [doi]
LID - 27758
AB  - Neuron-specific enolase (NSE) is a glycolytic isoenzyme found in mature neurons 
      and cells of neuronal origin. Injecting adeno-associated virus serotype 9 (AAV9) 
      vectors carrying the NSE promoter into the cerebellar cortex is likely to cause 
      the specific transduction of neuronal cells, such as Purkinje cells (PCs) and 
      interneurons, but not Bergmann glia (BG). However, we found BG-predominant 
      transduction without PC transduction along a traumatic needle tract for viral 
      injection. The enhancement of neuroinflammation by the co-application of 
      lipopolysaccharide (LPS) with AAV9 significantly expanded the BG-predominant area 
      concurrently with the potentiated microglial activation. The BG-predominant 
      transduction was gradually replaced by the PC-predominant transduction as the 
      neuroinflammation dissipated. Experiments using glioma cell cultures revealed 
      significant activation of the NSE promoter due to glucose deprivation, suggesting 
      that intracellularly stored glycogen is metabolized through the glycolytic 
      pathway for energy. Activation of the glycolytic enzyme promoter in BG 
      concurrently with inactivation in PC may have pathophysiological significance for 
      the production of lactate in activated BG and the utilization of lactate, which 
      is provided by the BG-PC lactate shuttle, as a primary energy resource in injured 
      PCs.
FAU - Sawada, Yusuke
AU  - Sawada Y
AD  - Department of Neurophysiology &Neural Repair, Gunma University Graduate School of 
      Medicine, Maebashi, Gunma 371-8511, Japan.
FAU - Konno, Ayumu
AU  - Konno A
AD  - Department of Neurophysiology &Neural Repair, Gunma University Graduate School of 
      Medicine, Maebashi, Gunma 371-8511, Japan.
FAU - Nagaoka, Jun
AU  - Nagaoka J
AD  - Department of Neurophysiology &Neural Repair, Gunma University Graduate School of 
      Medicine, Maebashi, Gunma 371-8511, Japan.
FAU - Hirai, Hirokazu
AU  - Hirai H
AD  - Department of Neurophysiology &Neural Repair, Gunma University Graduate School of 
      Medicine, Maebashi, Gunma 371-8511, Japan.
AD  - Research Program for Neural Signalling, Division of Endocrinology, Metabolism and 
      Signal Research, Gunma University Initiative for Advanced Research, Maebashi, 
      Gunma 371-8511, Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160613
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
RN  - 0 (Lipopolysaccharides)
RN  - 33X04XA5AT (Lactic Acid)
RN  - EC 4.2.1.11 (Phosphopyruvate Hydratase)
SB  - IM
MH  - Animals
MH  - Cells, Cultured
MH  - Cerebellar Cortex/immunology/metabolism
MH  - Dependovirus/genetics
MH  - Genetic Vectors/administration & dosage
MH  - Inflammation/chemically induced/*genetics
MH  - Lactic Acid/metabolism
MH  - Lipopolysaccharides/adverse effects
MH  - Mice
MH  - Neuroglia/*immunology/metabolism
MH  - Phosphopyruvate Hydratase/*genetics
MH  - Promoter Regions, Genetic
MH  - Purkinje Cells/*immunology/metabolism
MH  - Rats
PMC - PMC4904196
EDAT- 2016/06/14 06:00
MHDA- 2018/04/27 06:00
PMCR- 2016/06/13
CRDT- 2016/06/14 06:00
PHST- 2016/01/20 00:00 [received]
PHST- 2016/05/23 00:00 [accepted]
PHST- 2016/06/14 06:00 [entrez]
PHST- 2016/06/14 06:00 [pubmed]
PHST- 2018/04/27 06:00 [medline]
PHST- 2016/06/13 00:00 [pmc-release]
AID - srep27758 [pii]
AID - 10.1038/srep27758 [doi]
PST - epublish
SO  - Sci Rep. 2016 Jun 13;6:27758. doi: 10.1038/srep27758.