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  1. Article ; Online: Mast cells as early responders in the regulation of acute blood-brain barrier changes after cerebral ischemia and hemorrhage.

    Lindsberg, Perttu Johannes / Strbian, Daniel / Karjalainen-Lindsberg, Marja-Liisa

    Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism

    2010  Volume 30, Issue 4, Page(s) 689–702

    Abstract: The inflammatory response triggered by stroke has been viewed as harmful, focusing on the influx and migration of blood-borne leukocytes, neutrophils, and macrophages. This review hypothesizes that the brain and meninges have their own resident cells ... ...

    Abstract The inflammatory response triggered by stroke has been viewed as harmful, focusing on the influx and migration of blood-borne leukocytes, neutrophils, and macrophages. This review hypothesizes that the brain and meninges have their own resident cells that are capable of fast host response, which are well known to mediate immediate reactions such as anaphylaxis, known as mast cells (MCs). We discuss novel research suggesting that by acting rapidly on the cerebral vessels, this cell type has a potentially deleterious role in the very early phase of acute cerebral ischemia and hemorrhage. Mast cells should be recognized as a potent inflammatory cell that, already at the outset of ischemia, is resident within the cerebral microvasculature. By releasing their cytoplasmic granules, which contain a host of vasoactive mediators such as tumor necrosis factor-alpha, histamine, heparin, and proteases, MCs act on the basal membrane, thus promoting blood-brain barrier (BBB) damage, brain edema, prolonged extravasation, and hemorrhage. This makes them a candidate for a new pharmacological target in attempts to even out the inflammatory responses of the neurovascular unit, and to stabilize the BBB after acute stroke.
    MeSH term(s) Animals ; Antigens, CD/metabolism ; Astrocytes/cytology ; Astrocytes/metabolism ; Basement Membrane/metabolism ; Blood-Brain Barrier/physiology ; Blood-Brain Barrier/physiopathology ; Brain/cytology ; Brain/immunology ; Brain/pathology ; Brain Ischemia/immunology ; Brain Ischemia/pathology ; Brain Ischemia/physiopathology ; Cerebral Hemorrhage/immunology ; Cerebral Hemorrhage/pathology ; Cerebral Hemorrhage/physiopathology ; Cerebrovascular Circulation ; Endothelial Cells/metabolism ; Fibrinolysis ; Humans ; Mast Cells/cytology ; Mast Cells/metabolism ; Neurons/cytology ; Neurons/metabolism ; Peptide Hydrolases/metabolism
    Chemical Substances Antigens, CD ; Peptide Hydrolases (EC 3.4.-)
    Language English
    Publishing date 2010-01-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 604628-9
    ISSN 1559-7016 ; 0271-678X
    ISSN (online) 1559-7016
    ISSN 0271-678X
    DOI 10.1038/jcbfm.2009.282
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1663: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Low-expression variant of fatty acid-binding protein 4 favors reduced manifestations of atherosclerotic disease and increased plaque stability.

    Saksi, Jani / Ijäs, Petra / Mäyränpää, Mikko I / Nuotio, Krista / Isoviita, Pia M / Tuimala, Jarno / Lehtonen-Smeds, Erno / Kaste, Markku / Jula, Antti / Sinisalo, Juha / Nieminen, Markku S / Lokki, Marja-Liisa / Perola, Markus / Havulinna, Aki S / Salomaa, Veikko / Kettunen, Johannes / Jauhiainen, Matti / Kovanen, Petri T / Lindsberg, Perttu J

    Circulation. Cardiovascular genetics

    2014  Volume 7, Issue 5, Page(s) 588–598

    Abstract: Background: Fatty acid-binding protein 4 (FABP4 or aP2 in mice) has been identified as a key regulator of core aspects of cardiometabolic disorders, including lipotoxic endoplasmic reticulum stress in macrophages. A functional promoter polymorphism ( ... ...

    Abstract Background: Fatty acid-binding protein 4 (FABP4 or aP2 in mice) has been identified as a key regulator of core aspects of cardiometabolic disorders, including lipotoxic endoplasmic reticulum stress in macrophages. A functional promoter polymorphism (rs77878271) of human FABP4 gene has been described resulting in reduced FABP4 transcription.
    Methods and results: We investigated the effects of this low-expression variant of FABP4 on cardiovascular morbidity and carotid atherosclerosis on a population level (n=7491) and in patient cohorts representing endarterectomized patients with advanced carotid atherosclerosis (n=92) and myocardial infarction (n=3432). We found that the low-expression variant was associated with decreased total cholesterol levels (P=0.006) with the largest reduction in variant allele homozygotes. Obese variant allele carriers also showed reduced carotid intima-media thickness (P=0.010) and lower prevalence of carotid plaques (P=0.060). Consistently, the variant allele homozygotes showed 8-fold lower odds for myocardial infarction (P=0.019; odds ratio, 0.12; 95% confidence interval, 0.003-0.801). Within the carotid plaques, the variant allele was associated with a 3.8-fold reduction in FABP4 transcription (P=0.049) and 2.7-fold reduction in apoptosis (activated caspase 3; P=0.043). Furthermore, the variant allele was enriched to patients with asymptomatic carotid stenosis (P=0.038). High FABP4 expression in the carotid plaques was associated with lipid accumulation, intraplaque hemorrhages, plaque ulcerations, and phosphoactivated endoplasmic reticulum stress markers.
    Conclusions: Our results reveal FABP4 rs77878271 as a novel variant affecting serum total cholesterol levels and cardiovascular risk. A therapeutic regimen reducing FABP4 expression within the atherosclerotic plaque may promote lesion stability through modulation of endoplasmic reticulum stress signaling, and attenuation of apoptosis, lipid burden, and inflammation.
    MeSH term(s) Aged ; Alleles ; Cardiovascular Diseases/blood ; Cardiovascular Diseases/genetics ; Carotid Arteries/pathology ; Endarterectomy ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum Stress ; Enzyme-Linked Immunosorbent Assay ; Fatty Acid-Binding Proteins/genetics ; Female ; Finland ; Genetic Variation ; Genotype ; Homozygote ; Humans ; Inflammation/blood ; Lipids/blood ; Macrophages/metabolism ; Male ; Middle Aged ; Odds Ratio ; Plaque, Atherosclerotic/blood ; Plaque, Atherosclerotic/genetics ; Polymorphism, Genetic ; Promoter Regions, Genetic ; Transcription, Genetic
    Chemical Substances FABP4 protein, human ; Fatty Acid-Binding Proteins ; Lipids
    Language English
    Publishing date 2014-10
    Publishing country United States
    Document type Journal Article ; Meta-Analysis ; Research Support, Non-U.S. Gov't
    ZDB-ID 2477394-3
    ISSN 1942-3268 ; 1942-325X
    ISSN (online) 1942-3268
    ISSN 1942-325X
    DOI 10.1161/CIRCGENETICS.113.000499
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6731: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
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