Chrysanthy Ikonomidou

Dr. Chrysanthy Ikonomidou

University of Wisconsin Madison, USA
orcid

Research Focus & Metrics

Academic Career Length

36Years (1991-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

View All Publications
1 May 2003 in Annals of the New York Academy of Sciences
Verified
Journal Article
Closed access
PDF file
PBPetra Bittigau
Petra Bittigau
MSMarco Sifringer
Marco Sifringer
CIChrysanthy Ikonomidou
Chrysanthy Ikonomidou

15 April 2011 in Antioxidants & Redox Signaling
Verified
Journal Article
Closed access
CIChrysanthy Ikonomidou
Chrysanthy Ikonomidou
AKAngela M. Kaindl
Angela M. Kaindl
The developing brain is particularly vulnerable to reactive oxygen and reactive nitrogen species–mediated damage because of its high concentrations of unsaturated fatty acids, high rate of oxygen consumption, low concentrations of antioxidants, high content of metals catalyzing free radical formation, and large proportion of sensitive immature cells. In this review, we outline the dynamic changes of energy resources, metabolic requirements, and endogenous free radical scavenging systems during physiologic brain development. We further discuss the involvement of oxidative stress in the pathogenesis of neuronal death after exposure of the infant brain to hyperoxia, hypoxia/ischemia, sedative drugs, ethanol, and mechanical trauma. Several approaches have been developed to combat oxidative stress, but neuroprotective treatment strategies are limited in the clinical setting. Antioxid. Redox Signal. 14, 1535–1550.

14 June 2009 in Histochemistry and Cell Biology
Verified
Journal Article
Closed access
PDF file
ASAndrzej Stepulak
Andrzej Stepulak
HLHella Luksch
Hella Luksch
CGChristine Gebhardt
Christine Gebhardt
OUOrtrud Uckermann
Ortrud Uckermann
JMJenny Marzahn
Jenny Marzahn
CIChrysanthy Ikonomidou
Chrysanthy Ikonomidou

1 October 2008 in Annals of Neurology
Verified
Journal Article
Closed access
PDF file
VSVanya G. Stefovska
Vanya G. Stefovska
OUOrtrud Uckermann
Ortrud Uckermann
Mirosław CzuczwarMirosław Czuczwar
Mirosław Czuczwar
MSMartin Smitka
Martin Smitka
PCPiotr Czuczwar
Piotr Czuczwar
CIChrysanthy Ikonomidou
Chrysanthy Ikonomidou

1 January 2010 in Epilepsy Research
Verified
Journal Article
Closed access
CIChrysanthy Ikonomidou
Chrysanthy Ikonomidou
LTLechoslaw Turski
Lechoslaw Turski

17 October 2005 in Proceedings of the National Academy of Sciences
Verified
Journal Article
Closed access
ASAndrzej Stepulak
Andrzej Stepulak
MSMarco Sifringer
Marco Sifringer
WRWojciech Rzeski
Wojciech Rzeski
Stefanie EndesfelderStefanie Endesfelder
Stefanie Endesfelder
AGAlexander Gratopp
Alexander Gratopp
CIChrysanthy Ikonomidou
Chrysanthy Ikonomidou
Glutamate antagonists limit the growth of human cancersin vitro. The mechanism of anticancer action of NMDA antagonists is not known, however. In this article, we report that the NMDA antagonist dizocilpine inhibits the extracellular signal-regulated kinase 1/2 pathway, an intracellular signaling cascade that is activated by growth factors and controls the proliferation of cancer cells. Dizocilpine reduces the phosphorylation of cAMP-responsive element binding protein, suppresses the expression of cyclin D1, up-regulates the cell cycle regulators and tumor suppressor proteins p21 and p53, and increases the number of lung adenocarcinoma cells in the G2and S phases of the cell cycle. Silencing of the tumor suppressor protein p21 abolishes antiproliferative action of dizocilpine. Consistent with inhibition of the extracellular signal-regulated kinase 1/2-signaling cascade, dizocilpine reverses the stimulation of proliferation induced by epidermal, insulin, and basic fibroblast growth factors in lung adenocarcinoma cells. Furthermore, dizocilpine prolongs the survival of mice with metastatic lung adenocarcinoma and slows the growth of neuroblastoma and rhabdomyosarcoma in mice. These findings reveal the mechanism of antiproliferative action of dizocilpine and indicate that it may be useful in the therapy of human cancers.