| Current
Neurovascular Research
ISSN: 1567-2026
Current Neurovascular Research
Volume 7, Number 1, February 2010
Contents
ORIGINAL ARTICLES
Haptoglobin Phenotype Correlates with the Extent of Cerebral
Deep White Matter Lesions in Hypertensive Patients
Pp. 1-5
Julie Staals, Léon H.G. Henskens, Joris R. Delanghe,
Robert J. van Oostenbrugge, Alfons G. Kessels, Abraham A.
Kroon, Peter W. de Leeuw and Jan Lodder
[Abstract] [Purchase
Article] [PMID:
20158468 PubMed - indexed for MEDLINE]
Characterization of Endogenous Neural Progenitor Cells
after Experimental Ischemic Stroke Pp. 6-14
Chiung-Chyi Shen, Yi-Chin Yang, Ming-Tsang Chiao, Wen-Yu
Cheng, Yuang-Seng Tsuei and Jiunn-Liang Ko
[Abstract] [Purchase
Article] [PMID:
20158467 PubMed - indexed for MEDLINE]
Iron Leads to Memory Impairment that is Associated
with a Decrease in Acetylcholinesterase Pathways
Pp. 15-22
Vinícius P. Perez, Maria Noêmia M. de Lima,
Rosane S. da Silva, Arethuza S. Dornelles, Gustavo Vedana,
Maurício R. Bogo, Carla D. Bonan and Nadja
Schröder
[Abstract] [Purchase
Article] [PMID:
20158466 PubMed - indexed for MEDLINE]
Nitric Oxide Production during Cerebral Ischemia and
Reperfusion in eNOS- and nNOS-Knockout Mice Pp. 23-31
Yasuo Ito, Takeshi Ohkubo, Yoshio Asano, Kimihiko Hattori,
Tomokazu Shimazu, Masamizu Yamazato, Harumitsu Nagoya, Yuji
Kato and Nobuo Araki
[Abstract] [Full
text article] [PMID:
20158465 PubMed - indexed for MEDLINE]
Real Time Analysis of Neurotransmitters in the Brain
using a Micro-Electrode System Pp. 32-38
Suw Young Ly, Hwa Jin Heo and Min Jung Kim
[Abstract] [Purchase
Article] [PMID:
20158464 PubMed - indexed for MEDLINE]
Interleukin-1β
Plays a Role in the Activation of Peripheral Leukocytes after
Blood-Brain Barrier Rupture in the Course of Subarachnoid
Hemorrhage Pp. 39-48
Halina Jedrzejowska-Szypulka, Grazyna Straszak, Magdalena
Larysz-Brysz, Jacek Karpe, Wieslaw Marcol, Edyta Olakowska,
Izabella Woszczycka-Korczynska and Joanna Lewin-Kowalik
[Abstract] [Purchase
Article] [PMID:
20158463 PubMed - indexed for MEDLINE]
Human Tooth Germ Stem Cells Preserve Neuro-Protective
Effects after Long-Term Cryo-Preservation Pp. 49-58
Mehmet E. Yalvaç, Mustafa Ramazanoglu, Murat Tekguc,
Omer F. Bayrak, Aygul K. Shafigullina, Ilnur I. Salafutdinov,
Natalia L. Blatt, Andrey P. Kiyasov, Fikrettin Sahin, András
Palotás and Albert A. Rizvanov
[Abstract] [Purchase
Article] [PMID:
20158462 PubMed - indexed for MEDLINE]
REVIEW ARTICLE
Diabetes Mellitus: Channeling Care through
Cellular Discovery Pp. 59-74
Kenneth Maiese, Yan Chen Shang, Zhao Zhong Chong and
Jinling Hou
[Abstract] [Purchase
Article] [PMID:
20158461 PubMed - indexed for MEDLINE]
Abstracts
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[Purchase
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20158468 PubMed - indexed for MEDLINE]
Haptoglobin Phenotype Correlates with the Extent of Cerebral
Deep White Matter Lesions in Hypertensive Patients
Julie Staals, Léon H.G. Henskens, Joris R. Delanghe,
Robert J. van Oostenbrugge, Alfons G. Kessels, Abraham A.
Kroon, Peter W. de Leeuw and Jan Lodder
Cerebral white matter lesions (WMLs), due to small vessel
disease, can be regarded as an early “silent”
sign of hypertensive cerebral end-organ damage. As haptoglobin
(Hp) phenotype has earlier been associated with symptomatic
vascular disease, we now examined the relationship between
Hp phenotype and asymptomatic cerebral small vessel disease,
manifested by deep and periventricular WMLs, in hypertensive
patients.
We determined Hp phenotype using starch gel electrophoresis
in 152 hypertensive patients without symptomatic vascular
disease. We found 26 (17.1%) Hp1-1, 89 (58.6%) Hp2-1 and 37
(24.3%) Hp2-2. Volumes of deep and periventricular WMLs were
quantitatively measured on brain MR images. Patients were
ranked in 5 categories according to ascending WMLs volumes.
Compared to Hp2-2, Hp1-1 was associated with larger deep WMLs
volumes when adjusted for age, gender, brain volume, 24-hour
mean arterial pressure, duration of hypertension and previous
antihypertensive treatment (ordinal regression analysis, OR
2.77, 95%CI 1.08-7.11, p=0.034). No association was found
between Hp phenotype and periventricular WMLs.
Hp1-1 phenotype correlates with the extent of hypertensive
deep white matter damage. One of the possibilities is that
this is related to lower regenerating power against endothelial
injury in Hp1-1 individuals.
[Back to top] [Purchase
Article] [PMID:
20158467 PubMed - indexed for MEDLINE]
Characterization of Endogenous Neural Progenitor Cells
after Experimental Ischemic Stroke
Chiung-Chyi Shen, Yi-Chin Yang, Ming-Tsang Chiao, Wen-Yu
Cheng, Yuang-Seng Tsuei and Jiunn-Liang Ko
Neural progenitors cells are capable of promoting neurogenesis
after ischemic stroke in the adult mammalian brain; however
the function of these cells and their fate is still not clear.
Therefore the purpose of this study investigated the relationship
between neural progenitors and reactive astrocytes after middle
cerebral artery occlusion (MCAO). Brain infarction was induced
by occlusion of a right cerebral artery in male Wistar rats.
The fate of progenitor cells and the surrounding cells was
investigated by immunochemical staining for nestin, vimentin
and glial fibrillary acidic protein (GFAP) positive cells
at several locations. Vimentin and nestin positive cells were
observed in the ipsilateral subventricular zone (SVZ), striatum,
and cortex at 3 and 7 days after MCAO, but those cells were
not found at 28 days after ischemia. In contrast, reactive
astrocyte positive cells increased following MCAO. These reactive
astrocytes induced astrocytes differentiation of progenitor
cells and formed dense astroglioses surrounding the ischemic
lesion. Reactive astrocytes are thought to protect the penumbra
during brain ischemia. We examined which brain cell expressed
nestin and GFAP in the ipsilateral co-expression at 7 days
after MCAO, especially at the core of injury. These results
suggest that robust reactive astrocytes after MCAO were possibly
differentiation from the induced nestin-positive cells after
early ischemia.
[Back to top] [Purchase
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20158466 PubMed - indexed for MEDLINE]
Iron Leads to Memory Impairment that is Associated
with a Decrease in Acetylcholinesterase Pathways
Vinícius P. Perez, Maria Noêmia M. de Lima,
Rosane S. da Silva, Arethuza S. Dornelles, Gustavo Vedana,
Maurício R. Bogo, Carla D. Bonan and Nadja
Schröder
Increasing evidence indicates that excessive iron in selective
regions of the brain may be involved in the etiology of neurodegenerative
disorders. Accordingly, increased levels of iron have been
described in brain regions of patients in Parkinson's and
Alzheimer's diseases. We have characterized neonatal iron
loading in rodents as a novel experimental model that mimics
the brain iron accumulation observed in patients with neurodegenerative
diseases and produces severe cognitive impairment in the adulthood.
In the present study we have investigated the involvement
of the cholinergic system on iron-induced memory impairment.
The effects of a single administration of the acetylcholinesterase
(AChE) inhibitor galantamine or the muscarinic receptor agonist
oxotremorine on iron-induced memory deficits in rats were
examined. Male Wistar rats received vehicle or iron (10.0
mg/kg) orally at postnatal days 12 to 14. At the age of 2-3
months, animals were trained in a novel object recognition
task. Iron-treated rats showed long-term impairments in recognition
memory. The impairing effect was reversed by systemic administration
of galantamine (1 mg/kg) immediately after training. In addition,
iron-treated rats that received oxotremorine (0.5 mg/kg) showed
enhanced memory retention. Rats given iron showed a decreased
AChE activity in the striatum when compared to controls. The
results suggest that, at least in part, iron-induced cognitive
deficits are related to a dysfunction of cholinergic neural
transmission in the brain. These findings might have implications
for the development of novel therapeutic strategies aimed
at ameliorating cognitive decline associated with neurodegenerative
disorders.
[Back to top] [Full
text article] [PMID:
20158465 PubMed - indexed for MEDLINE]
Nitric Oxide Production during Cerebral Ischemia and
Reperfusion in eNOS- and nNOS-Knockout Mice
Yasuo Ito, Takeshi Ohkubo, Yoshio Asano, Kimihiko Hattori,
Tomokazu Shimazu, Masamizu Yamazato, Harumitsu Nagoya, Yuji
Kato and Nobuo Araki
The purpose of this study was to clarify the kinetics of nitric
oxide (NO) induced by either endothelial NO synthase (eNOS)
or neuronal NO synthase (nNOS) after transient global forebrain
ischemia. We investigated NO production and ischemic changes
to hippocampal CA1 neurons in eNOS knockout (-/-) mice and
nNOS (-/-) mice during cerebral ischemia and reperfusion.
NO production was continuously monitored by in vivo
microdialysis. Global forebrain ischemia was produced by occlusion
of both common carotid arteries for 10 minutes. Levels of
nitrite (NO2 -) and nitrate
(NO3 -), as NO metabolites,
in dialysate were determined using the Griess reaction. Two
hours after the start of reperfusion, animals were perfused
with 4% paraformaldehyde. Hippocampal CA1 neurons were divided
into three phases (severely ischemic, moderately ischemic,
surviving), and the ratio of surviving neurons to degenerated
neurons was calculated as the survival rate. The relative
cerebral blood flow (rCBF) was significantly higher in nNOS
(-/-) mice than in control mice after reperfusion. Levels
of NO3 - were significantly
lower in eNOS (-/-) mice and nNOS (-/-) mice than in control
mice during ischemia and reperfusion. NO3
- levels were significantly lower in nNOS (-/-) mice than
in eNOS (-/-) mice after the start of reperfusion. Survival
rate tended to be higher in nNOS (-/-) mice than in control
mice, but not significantly. These in vivo data suggest
that NO production in the striatum after reperfusion is closely
related to activities of both nNOS and eNOS, and is mainly
related to nNOS following reperfusion.
Theme: Disorders of the nervous system.
Topic: Ischemia.
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Article] [PMID:
20158464 PubMed - indexed for MEDLINE]
Real Time Analysis of Neurotransmitters in the Brain
using a Micro-Electrode System
Suw Young Ly, Hwa Jin Heo and Min Jung Kim
Neurotransmitters catechol and dopamine analogy levels are
related to the systematic nerve activity. This assay was performed
by using cyclic voltammetry (CV) and square wave (SW) stripping
voltammetry, while optimization was performed by the carbon
fiber microelectrode (CFME) with wire-type reference and counter
electrodes. In the electrolyte solutions, the analytical parameters
of catechol were as follows: 8.5 pH, -0.4 V anodic, 0.3 V
cathodic, 15s deposition time, 15 Hz SW frequency, 25 mV SW
amplitude and incremental potential of 4 mV, under optimal
conditions, working ranges were 0-50 mgL-1
CV, 0.01-50 mgL-1 cathodic,
and 1-13 mgL-1 anodic, the
relative standard deviation was 0.02 %, n = 15 using 0.5 mgL-1
and the detection limit was 4.0 ugL-1.
It can be used for in vivo direct analysis. Here,
diagnostic applications were performed in the brain skeleton
of living cells in real time. The developed techniques can
be useful for nerve control and signal detections.
[Back to top] [Purchase
Article] [PMID:
20158463 PubMed - indexed for MEDLINE]
Interleukin-1β
Plays a Role in the Activation of Peripheral Leukocytes after
Blood-Brain Barrier Rupture in the Course of Subarachnoid
Hemorrhage
Halina Jedrzejowska-Szypulka, Grazyna Straszak, Magdalena
Larysz-Brysz, Jacek Karpe, Wieslaw Marcol, Edyta Olakowska,
Izabella Woszczycka-Korczynska and Joanna Lewin-Kowalik
Subarachnoid hemorrhage (SAH) develops when extravasated arterial
blood enters subarachnoid space and mixes with cerebrospinal
fluid. As a result, many pathologies develop, including increase
in brain-blood barrier (BBB) permeability and activation of
peripheral leukocytes, that in turn augment immuno-inflammatory
response, considered as the cause of numerous complications
following SAH.
In the study, we examined the role of one of the major cytokines,
interleukin 1-beta (IL-1beta), in the BBB rupture and subsequent
migration of leukocytes into central nervous system (CNS)
after experimental SAH in adult rats. SAH was produced by
injection of 150 uL of autologous arterial blood into cisterna
magna. In 50% of animals, IL-1beta activity was inhibited
by intracerebroventricular administration of anti-rat IL-1beta
antibodies (SAH’ groups). Control group consisted of
sham-operated rats. Ninety minutes or 24 hrs following surgery,
blood samples were taken, then animals were perfused transcardially
and whole brains were collected. Three major populations of
leukocytes present at brain stem and frontal part of the brain
– granulocytes, monocytes/macrophages and lymphocytes
– were labeled with appropriate antibodies. S-100B protein
concentration in the serum, a marker of BBB permeability,
was also measured. Neutralization of IL-1beta activity reduced
elevated S-100B level and the number of leukocytes found within
the CNS, however these changes were not uniformly significant
among different subgroups. The results demonstrate an important
role of IL-1beta in the BBB damage and leukocyte migration
into the CNS subarachnoid hemorrhage.
[Back to top] [Purchase
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20158462 PubMed - indexed for MEDLINE]
Human Tooth Germ Stem Cells Preserve Neuro-Protective
Effects after Long-Term Cryo-Preservation
Mehmet E. Yalvaç, Mustafa Ramazanoglu, Murat Tekguc,
Omer F. Bayrak, Aygul K. Shafigullina, Ilnur I. Salafutdinov,
Natalia L. Blatt, Andrey P. Kiyasov, Fikrettin Sahin, András
Palotás and Albert A. Rizvanov
The use of mesenchymal stem cells (MSCs) has been shown to
be promising in chronic disorders such as diabetes, Alzheimer’s
dementia, Parkinson’s disease, spinal cord injury and
brain ischemia. Recent studies revealed that human tooth germs
(hTG) contain MSCs which can be easily isolated, expanded
and cryo-preserved. In this report, we isolated human tooth
germ stem cells (hTGSCs) with MSC characteristics from third
molar tooth germs, cryo-preserved them at -800C
for 6 months, and evaluated for their surface antigens, expression
of pluri-potency associated genes, differentiation capacity,
karyotype, and proliferation rate. These characteristics were
compared to their non-frozen counterparts. In addition, neuro-protective
effects of cryo-preserved cells on neuro-blastoma SH-SY5Y
cells were also assessed after exposure to stress conditions
induced by hydrogen-peroxide (oxidative stress) and paclitaxel
(microtubule stabilizing mitotic inhibitor). After long term
cryo-preservation hTGSCs expressed surface antigens CD29,
CD73, CD90, CD105, and CD166, but not CD34, CD45 or CD133,
which was typical for non-frozen hTGSCs. Cryo-preserved hTGSCs
were able to differentiate into osteo-, adipo- and neuro-genic
cells. They also showed normal karyotype after high number
of population doublings and unchanged proliferation rate.
On the other hand, cryo-preserved cells demonstrated a tendency
for lower level of pluri-potency associated gene expression
(nanog, oct4, sox2, klf4, c-myc) than non-frozen
hTGSCs. hTGSCs conditioned media increased survival of SH-SY5Y
cells exposed to oxidative stress or paclitaxel. These findings
confirm that hTGSCs preserve their major characteristics and
exert neuro-protection after long-term cryo-preservation,
suggesting that hTGSCs, harvested from young individuals and
stored for possible use later as they grow old, might be employed
in cellular therapy of age-related degenerative disorders.
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[Purchase
Article] [PMID:
20158461 PubMed - indexed for MEDLINE]
Diabetes Mellitus: Channeling Care through Cellular Discovery
Kenneth Maiese, Yan Chen Shang, Zhao Zhong Chong and
Jinling Hou
Diabetes mellitus (DM) impacts a significant portion
of the world’s population and care for this disorder
places an economic burden on the gross domestic product for
any particular country. Furthermore, both Type 1 and Type
2 DM are becoming increasingly prevalent and there is increased
incidence of impaired glucose tolerance in the young. The
complications of DM are protean and can involve multiple systems
throughout the body that are susceptible to the detrimental
effects of oxidative stress and apoptotic cell injury. For
these reasons, innovative strategies are necessary for the
implementation of new treatments for DM that are generated
through the further understanding of cellular pathways that
govern the pathological consequences of DM. In particular,
both the precursor for the coenzyme ß-nicotinamide
adenine dinucleotide (NAD+),
nicotinamide, and the growth factor erythropoietin offer novel
platforms for drug discovery that involve cellular metabolic
homeostasis and inflammatory cell control. Interestingly,
these agents and their tightly associated pathways that consist
of cell cycle regulation, protein kinase B, forkhead transcription
factors, and Wnt signaling also function in a broader sense
as biomarkers for disease onset and progression.
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