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 S. Prough

doi:10.1016/j.neulet.2003.10.074

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 S. Prough

Anesthesiology

Research output: Contribution to journal › Article › peer-review

55 Scopus citations

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 language	English (US)
Pages (from-to)	221-225
Number of pages	5
Journal	Neuroscience Letters
Volume	355
Issue number	3
DOIs	https://doi.org/10.1016/j.neulet.2003.10.074
State	Published - Jan 30 2004

Keywords

Apoptosis
Gene expression
Neuroprotection
Traumatic brain injury
Zinc

ASJC Scopus subject areas

General Neuroscience

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10.1016/j.neulet.2003.10.074

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@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 Prough, \{Donald S.\}",

note = "Funding Information: This study was funded by a grant from the University of Texas Medical Branch John Sealy Memorial Endowment Fund for Biomedical Research \#2558-01 (to H.L.H.) and NIH grant NS19355 (to D.S.D.), and supported in part by NIH grants NS40215, NS38585, and NS42882 (to C.J.F.). We thank Dr Marcia Saban and Becky Nguyen for their valuable assistance with the microarray data analysis, Dr Cheng Lin for his help with the RPAs, Christy Perry for her assistance in scanning and analyzing the microarray data and for preparing figures for the manuscript, and Jordan Kicklighter and Lauren Tunnell for editing and preparing the manuscript.",

year = "2004",

month = jan,

day = "30",

doi = "10.1016/j.neulet.2003.10.074",

language = "English (US)",

volume = "355",

pages = "221--225",

journal = "Neuroscience Letters",

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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 S.

N1 - Funding Information: This study was funded by a grant from the University of Texas Medical Branch John Sealy Memorial Endowment Fund for Biomedical Research #2558-01 (to H.L.H.) and NIH grant NS19355 (to D.S.D.), and supported in part by NIH grants NS40215, NS38585, and NS42882 (to C.J.F.). We thank Dr Marcia Saban and Becky Nguyen for their valuable assistance with the microarray data analysis, Dr Cheng Lin for his help with the RPAs, Christy Perry for her assistance in scanning and analyzing the microarray data and for preparing figures for the manuscript, and Jordan Kicklighter and Lauren Tunnell for editing and preparing the manuscript.

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

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AN - SCOPUS:1542347159

SN - 0304-3940

VL - 355

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JO - Neuroscience Letters

JF - Neuroscience Letters

IS - 3

ER -

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

Abstract

Keywords

ASJC Scopus subject areas

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