PMID- 29648986
OWN - NLM
STAT- MEDLINE
DCOM- 20191111
LR  - 20191111
IS  - 1557-9042 (Electronic)
IS  - 0897-7151 (Print)
IS  - 0897-7151 (Linking)
VI  - 35
IP  - 17
DP  - 2018 Sep 1
TI  - A Single Primary Blast-Induced Traumatic Brain Injury in a Rodent Model Causes 
      Cell-Type Dependent Increase in Nicotinamide Adenine Dinucleotide Phosphate 
      Oxidase Isoforms in Vulnerable Brain Regions.
PG  - 2077-2090
LID - 10.1089/neu.2017.5358 [doi]
AB  - Blast-induced traumatic brain injury (bTBI) is a leading cause of morbidity in 
      soldiers on the battlefield and in training sites with long-term neurological and 
      psychological pathologies. Previous studies from our laboratory demonstrated 
      activation of oxidative stress pathways after blast injury, but their 
      distribution among different brain regions and their impact on the pathogenesis 
      of bTBI have not been explored. The present study examined the protein expression 
      of two isoforms: nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 1 
      and 2 (NOX1, NOX2), corresponding superoxide production, a downstream event of 
      NOX activation, and the extent of lipid peroxidation adducts of 4-hydroxynonenal 
      (4HNE) to a range of proteins. Brain injury was evaluated 4 h after the 
      shock-wave exposure, and immunofluorescence signal quantification was performed 
      in different brain regions. Expression of NOX isoforms displayed a differential 
      increase in various brain regions: in hippocampus and thalamus, there was the 
      highest increase of NOX1, whereas in the frontal cortex, there was the highest 
      increase of NOX2 expression. Cell-specific analysis of changes in NOX expression 
      with respect to corresponding controls revealed that blast resulted in a higher 
      increase of NOX1 and NOX 2 levels in neurons compared with astrocytes and 
      microglia. Blast exposure also resulted in increased superoxide levels in 
      different brain regions, and such changes were reflected in 4HNE protein adduct 
      formation. Collectively, this study demonstrates that primary blast TBI induces 
      upregulation of NADPH oxidase isoforms in different regions of the brain 
      parenchyma and that neurons appear to be at higher risk for oxidative damage 
      compared with other neural cells.
FAU - Rama Rao, Kakulavarapu V
AU  - Rama Rao KV
AD  - 1 Center for Injury Biomechanics, Materials, and Medicine, Department of 
      Biomedical Engineering, New Jersey Institute of Technology , Newark, New Jersey.
FAU - Iring, Stephanie
AU  - Iring S
AD  - 1 Center for Injury Biomechanics, Materials, and Medicine, Department of 
      Biomedical Engineering, New Jersey Institute of Technology , Newark, New Jersey.
FAU - Younger, Daniel
AU  - Younger D
AD  - 1 Center for Injury Biomechanics, Materials, and Medicine, Department of 
      Biomedical Engineering, New Jersey Institute of Technology , Newark, New Jersey.
FAU - Kuriakose, Matthew
AU  - Kuriakose M
AD  - 1 Center for Injury Biomechanics, Materials, and Medicine, Department of 
      Biomedical Engineering, New Jersey Institute of Technology , Newark, New Jersey.
FAU - Skotak, Maciej
AU  - Skotak M
AD  - 1 Center for Injury Biomechanics, Materials, and Medicine, Department of 
      Biomedical Engineering, New Jersey Institute of Technology , Newark, New Jersey.
FAU - Alay, Eren
AU  - Alay E
AD  - 1 Center for Injury Biomechanics, Materials, and Medicine, Department of 
      Biomedical Engineering, New Jersey Institute of Technology , Newark, New Jersey.
FAU - Gupta, Raj K
AU  - Gupta RK
AD  - 2 Department of Defense Blast Injury Research Program Coordinating Office, United 
      States Army Medical Research and Materiel Command , Fort Detrick, Maryland.
FAU - Chandra, Namas
AU  - Chandra N
AD  - 1 Center for Injury Biomechanics, Materials, and Medicine, Department of 
      Biomedical Engineering, New Jersey Institute of Technology , Newark, New Jersey.
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20180612
PL  - United States
TA  - J Neurotrauma
JT  - Journal of neurotrauma
JID - 8811626
RN  - 0 (Isoenzymes)
RN  - 11062-77-4 (Superoxides)
RN  - EC 1.6.3.- (Cybb protein, rat)
RN  - EC 1.6.3.- (NADPH Oxidase 1)
RN  - EC 1.6.3.- (NADPH Oxidase 2)
RN  - EC 1.6.3.- (NADPH Oxidases)
RN  - EC 1.6.3.- (NOX1 protein, rat)
SB  - IM
MH  - Animals
MH  - Astrocytes/metabolism
MH  - Blast Injuries/*metabolism
MH  - Brain Chemistry
MH  - Brain Injuries, Traumatic/*metabolism
MH  - Cerebellum/metabolism
MH  - Hippocampus/metabolism
MH  - Isoenzymes
MH  - Lipid Peroxidation
MH  - Male
MH  - NADPH Oxidase 1/biosynthesis/genetics
MH  - NADPH Oxidase 2/biosynthesis/genetics
MH  - NADPH Oxidases/*biosynthesis
MH  - Neurons/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Superoxides/metabolism
MH  - Thalamus/metabolism
PMC - PMC6098412
OTO - NOTNLM
OT  - 4-hydroxynonenal
OT  - NADPH oxidase
OT  - astrocytes
OT  - blast injury
OT  - microglia
OT  - neuron
OT  - oxidative stress
OT  - traumatic brain injury
COIS- No competing financial interests exist.
EDAT- 2018/04/13 06:00
MHDA- 2019/11/12 06:00
PMCR- 2018/09/01
CRDT- 2018/04/13 06:00
PHST- 2018/04/13 06:00 [pubmed]
PHST- 2019/11/12 06:00 [medline]
PHST- 2018/04/13 06:00 [entrez]
PHST- 2018/09/01 00:00 [pmc-release]
AID - 10.1089/neu.2017.5358 [pii]
AID - 10.1089/neu.2017.5358 [doi]
PST - ppublish
SO  - J Neurotrauma. 2018 Sep 1;35(17):2077-2090. doi: 10.1089/neu.2017.5358. Epub 2018 
      Jun 12.