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conferenceseries
.com
Volume 8, Issue 6
J Neurol Neurosci
ISSN: 2171-6625 Neuro, an open access journal
Neuroscience 2017
October 16-17, 2017
OCTOBER 16-17, 2017 OSAKA, JAPAN
17
TH
Global Neuroscience Conference
The detrimental roles of neutrophil gelatinase-associated lipocalin in ischemic stroke
Yi-Chinn Weng, Guona Wang, Yu-Chieh Wu and Wen-Hai Chou
National Health Research Institutes, Taiwan
I
schemic stroke is a major cause of death and long-term disability worldwide. Tissue plasminogen activator (tPA) is the only
drug approved for pharmacological intervention to reverse acute ischemic stroke, but reestablishment of circulation may
paradoxically initiate reperfusion injury. Activated immune cells (neutrophils, macrophages) infiltrate into ischemic brain tissue,
release free radicals, pro-inflammatory cytokines and proteins, thus causing brain edema, disruption of blood-brain barrier
(BBB) and neuronal cell death. Therefore, treatments that can inactivate these immune cells and limit stroke-reperfusion injuries
are urgently needed. Our recent results demonstrate that neutrophil gelatinase-associated lipocalin (NGAL) was acutely induced
in mice and humans after ischemic stroke and is an important mediator of stroke-reperfusion injury. Increased levels of NGAL
were observed in mouse serum as early as 1 hour after transient middle cerebral artery occlusion (tMCAo), reaching peak
levels at 23 hours. NGAL was also detected in neutrophils infiltrating into the ipsilateral hemisphere, as well as a subset of
astrocytes after tMCAo, but not in neurons and microglia. Cerebral infarctions, neurological deficits, infiltration of immune
cells, pro-inflammatory molecules and BBB permeability after tMCAo was significantly reduced in NGAL null mice. The plasma
concentration of NGAL was markedly elevated in patients with ischemic stroke. During a four year follow-up, patients with
higher levels of NGAL had higher mortality rates. These results demonstrate that NGAL is a neurotoxic factor secreted rapidly in
response to cerebral ischemia, suggesting its potential usage as an early stroke biomarker and a novel therapeutic target to reduce
stroke-reperfusion injury.
Biography
Yi-Chinn Weng has completed her PhD from Department of Molecular Medicine, University of Texas Health Science Center, San Antonio and Postdoctoral studies
from University of California, San Francisco. She has published several research papers in reputed journals including
Nature, Proceedings of the National Academy
of Sciences, Annals of Neurology
and
Journal of Biological Chemistry
.
wengyc050706@nhri.org.twYi-Chinn Weng et al., J Neurol Neurosci 2017, 8:6
DOI: 10.21767/2171-6625-C1-006