Protective effects of zinc chelation in traumatic brain injury correlate with upregulation of neuroprotective genes in rat brain

Helen Hellmich, Christopher J. Frederickson, Douglas Dewitt, Ricardo Saban, Margaret O. Parsley, Rachael Stephenson, Marco Velasco, Tatsuo Uchida, Megumi Shimamura, Donald Prough

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Chelation of excessive neuronal zinc ameliorates zinc neurotoxicity and reduces subsequent neuronal injury. To clarify the molecular mechanisms of this neuroprotective effect, we used a focused cDNA array of stress-response genes with zinc chelation (calcium EDTA) in our rat model of fluid percussion brain injury at 2 h, 24 h, and 7 days after injury. In parallel experiments, we compared neuronal cell death in TUNEL-stained brain sections in traumatized rats with and without calcium EDTA treatment. Zinc chelation induced the expression of several neuroprotective genes; neuroprotective gene expression correlated with substantially decreased numbers of TUNEL-positive cells.

Original languageEnglish (US)
Pages (from-to)221-225
Number of pages5
JournalNeuroscience Letters
Volume355
Issue number3
DOIs
StatePublished - Jan 30 2004

Fingerprint

Zinc
Up-Regulation
In Situ Nick-End Labeling
Brain
Edetic Acid
Genes
Calcium
Percussion
Wounds and Injuries
Neuroprotective Agents
Oligonucleotide Array Sequence Analysis
Brain Injuries
Cell Death
Gene Expression
Traumatic Brain Injury

Keywords

  • Apoptosis
  • Gene expression
  • Neuroprotection
  • Traumatic brain injury
  • Zinc

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Protective effects of zinc chelation in traumatic brain injury correlate with upregulation of neuroprotective genes in rat brain. / Hellmich, Helen; Frederickson, Christopher J.; Dewitt, Douglas; Saban, Ricardo; Parsley, Margaret O.; Stephenson, Rachael; Velasco, Marco; Uchida, Tatsuo; Shimamura, Megumi; Prough, Donald.

In: Neuroscience Letters, Vol. 355, No. 3, 30.01.2004, p. 221-225.

Research output: Contribution to journalArticle

Hellmich, Helen ; Frederickson, Christopher J. ; Dewitt, Douglas ; Saban, Ricardo ; Parsley, Margaret O. ; Stephenson, Rachael ; Velasco, Marco ; Uchida, Tatsuo ; Shimamura, Megumi ; Prough, Donald. / Protective effects of zinc chelation in traumatic brain injury correlate with upregulation of neuroprotective genes in rat brain. In: Neuroscience Letters. 2004 ; Vol. 355, No. 3. pp. 221-225.
@article{50ef64e3768f4f6198ac81af77296d46,
title = "Protective effects of zinc chelation in traumatic brain injury correlate with upregulation of neuroprotective genes in rat brain",
abstract = "Chelation of excessive neuronal zinc ameliorates zinc neurotoxicity and reduces subsequent neuronal injury. To clarify the molecular mechanisms of this neuroprotective effect, we used a focused cDNA array of stress-response genes with zinc chelation (calcium EDTA) in our rat model of fluid percussion brain injury at 2 h, 24 h, and 7 days after injury. In parallel experiments, we compared neuronal cell death in TUNEL-stained brain sections in traumatized rats with and without calcium EDTA treatment. Zinc chelation induced the expression of several neuroprotective genes; neuroprotective gene expression correlated with substantially decreased numbers of TUNEL-positive cells.",
keywords = "Apoptosis, Gene expression, Neuroprotection, Traumatic brain injury, Zinc",
author = "Helen Hellmich and Frederickson, {Christopher J.} and Douglas Dewitt and Ricardo Saban and Parsley, {Margaret O.} and Rachael Stephenson and Marco Velasco and Tatsuo Uchida and Megumi Shimamura and Donald Prough",
year = "2004",
month = "1",
day = "30",
doi = "10.1016/j.neulet.2003.10.074",
language = "English (US)",
volume = "355",
pages = "221--225",
journal = "Neuroscience Letters",
issn = "0304-3940",
publisher = "Elsevier Ireland Ltd",
number = "3",

}

TY - JOUR

T1 - Protective effects of zinc chelation in traumatic brain injury correlate with upregulation of neuroprotective genes in rat brain

AU - Hellmich, Helen

AU - Frederickson, Christopher J.

AU - Dewitt, Douglas

AU - Saban, Ricardo

AU - Parsley, Margaret O.

AU - Stephenson, Rachael

AU - Velasco, Marco

AU - Uchida, Tatsuo

AU - Shimamura, Megumi

AU - Prough, Donald

PY - 2004/1/30

Y1 - 2004/1/30

N2 - Chelation of excessive neuronal zinc ameliorates zinc neurotoxicity and reduces subsequent neuronal injury. To clarify the molecular mechanisms of this neuroprotective effect, we used a focused cDNA array of stress-response genes with zinc chelation (calcium EDTA) in our rat model of fluid percussion brain injury at 2 h, 24 h, and 7 days after injury. In parallel experiments, we compared neuronal cell death in TUNEL-stained brain sections in traumatized rats with and without calcium EDTA treatment. Zinc chelation induced the expression of several neuroprotective genes; neuroprotective gene expression correlated with substantially decreased numbers of TUNEL-positive cells.

AB - Chelation of excessive neuronal zinc ameliorates zinc neurotoxicity and reduces subsequent neuronal injury. To clarify the molecular mechanisms of this neuroprotective effect, we used a focused cDNA array of stress-response genes with zinc chelation (calcium EDTA) in our rat model of fluid percussion brain injury at 2 h, 24 h, and 7 days after injury. In parallel experiments, we compared neuronal cell death in TUNEL-stained brain sections in traumatized rats with and without calcium EDTA treatment. Zinc chelation induced the expression of several neuroprotective genes; neuroprotective gene expression correlated with substantially decreased numbers of TUNEL-positive cells.

KW - Apoptosis

KW - Gene expression

KW - Neuroprotection

KW - Traumatic brain injury

KW - Zinc

UR - http://www.scopus.com/inward/record.url?scp=1542347159&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=1542347159&partnerID=8YFLogxK

U2 - 10.1016/j.neulet.2003.10.074

DO - 10.1016/j.neulet.2003.10.074

M3 - Article

C2 - 14732471

AN - SCOPUS:1542347159

VL - 355

SP - 221

EP - 225

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

IS - 3

ER -