Excitatory and Mitogenic Signaling in Cell Death, Blood-brain Barrier Breakdown, and BBB Repair after Intracerebral Hemorrhage

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15 Citations (Scopus)

Abstract

Intracerebral hemorrhage (ICH) results in the release of a large number of endogenous molecules, including glutamate, Ca 2+, ROS, thrombin, heme, iron, TNF-α, and others. These molecules participate in excitatory and mitogenic signaling transduction in which N-methyl-d-aspartate (NMDA) receptors and Src family kinases (SFKs) are implicated. Mitogenic signaling initiates the cell cycle for normal cell division of microglia and neural progenitor cells, whereas aberrant mitogenic signaling causes toxicity, killing neurons, astrocytes, and brain microvascular endothelial cells in neurological diseases including ICH. In this review, we summarize (1) how SFKs modulate NMDA receptors to kill neurons following ICH and (2) how SFKs modulate mitogenic signaling transduction to kill neurons and play a role in disrupting the blood-brain barrier (BBB) immediately following ICH and in repairing the BBB during the recovery phases weeks following ICH.

Original languageEnglish (US)
Pages (from-to)62-69
Number of pages8
JournalTranslational Stroke Research
Volume3
Issue numberSUPPL. 1
DOIs
StatePublished - Jul 2012

Fingerprint

Cerebral Hemorrhage
Blood-Brain Barrier
Cell Death
src-Family Kinases
Neurons
Microglia
Heme
Thrombin
Astrocytes
Cell Division
Glutamic Acid
Cell Cycle
Stem Cells
Iron
Endothelial Cells
Brain
aspartic acid receptor

Keywords

  • Blood-brain barrier
  • Cell cycle
  • Excitotoxicty
  • Intracerebral hemorrhage
  • Mitogenic signaling
  • NMDA receptors
  • Src kinases

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)
  • Cardiology and Cardiovascular Medicine

Cite this

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title = "Excitatory and Mitogenic Signaling in Cell Death, Blood-brain Barrier Breakdown, and BBB Repair after Intracerebral Hemorrhage",
abstract = "Intracerebral hemorrhage (ICH) results in the release of a large number of endogenous molecules, including glutamate, Ca 2+, ROS, thrombin, heme, iron, TNF-α, and others. These molecules participate in excitatory and mitogenic signaling transduction in which N-methyl-d-aspartate (NMDA) receptors and Src family kinases (SFKs) are implicated. Mitogenic signaling initiates the cell cycle for normal cell division of microglia and neural progenitor cells, whereas aberrant mitogenic signaling causes toxicity, killing neurons, astrocytes, and brain microvascular endothelial cells in neurological diseases including ICH. In this review, we summarize (1) how SFKs modulate NMDA receptors to kill neurons following ICH and (2) how SFKs modulate mitogenic signaling transduction to kill neurons and play a role in disrupting the blood-brain barrier (BBB) immediately following ICH and in repairing the BBB during the recovery phases weeks following ICH.",
keywords = "Blood-brain barrier, Cell cycle, Excitotoxicty, Intracerebral hemorrhage, Mitogenic signaling, NMDA receptors, Src kinases",
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N2 - Intracerebral hemorrhage (ICH) results in the release of a large number of endogenous molecules, including glutamate, Ca 2+, ROS, thrombin, heme, iron, TNF-α, and others. These molecules participate in excitatory and mitogenic signaling transduction in which N-methyl-d-aspartate (NMDA) receptors and Src family kinases (SFKs) are implicated. Mitogenic signaling initiates the cell cycle for normal cell division of microglia and neural progenitor cells, whereas aberrant mitogenic signaling causes toxicity, killing neurons, astrocytes, and brain microvascular endothelial cells in neurological diseases including ICH. In this review, we summarize (1) how SFKs modulate NMDA receptors to kill neurons following ICH and (2) how SFKs modulate mitogenic signaling transduction to kill neurons and play a role in disrupting the blood-brain barrier (BBB) immediately following ICH and in repairing the BBB during the recovery phases weeks following ICH.

AB - Intracerebral hemorrhage (ICH) results in the release of a large number of endogenous molecules, including glutamate, Ca 2+, ROS, thrombin, heme, iron, TNF-α, and others. These molecules participate in excitatory and mitogenic signaling transduction in which N-methyl-d-aspartate (NMDA) receptors and Src family kinases (SFKs) are implicated. Mitogenic signaling initiates the cell cycle for normal cell division of microglia and neural progenitor cells, whereas aberrant mitogenic signaling causes toxicity, killing neurons, astrocytes, and brain microvascular endothelial cells in neurological diseases including ICH. In this review, we summarize (1) how SFKs modulate NMDA receptors to kill neurons following ICH and (2) how SFKs modulate mitogenic signaling transduction to kill neurons and play a role in disrupting the blood-brain barrier (BBB) immediately following ICH and in repairing the BBB during the recovery phases weeks following ICH.

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KW - Cell cycle

KW - Excitotoxicty

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KW - Mitogenic signaling

KW - NMDA receptors

KW - Src kinases

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