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The cellular and genomic response of an immortalized microglia cell line (BV2) to concentrated ambient particulate matter.

The cellular and genomic response of an immortalized microglia cell line (BV2) to concentrated ambient particulate matter. Research Abstract Details 

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  • The cellular and genomic response of an immortalized microglia cell line (BV2) to concentrated ambient particulate matter. Abstract Text:

    preethi samaPreethi Sama,thomas c longThomas C Long,susan hesterSusan Hester,julianne tajubaJulianne Tajuba,joel parkerJoel Parker,lung-chi chenLung-Chi Chen,bellina veronesiBellina Veronesi,

    Ambient particulate matter (PM) damages pulmonary tissue through oxidative stress (OS) pathways. Several reports indicate that the brain is another affected target of PM exposure. Since microglia (brain macrophages) are critical to OS-mediated neurodegeneration, the cellular and genomic response of immortalized mouse microglia (BV2) was examined in response to fine (or= 250 microg/ml) and depolarized mitochondrial membranes (>or= 6 microg/ml) within 15 min of exposure. HP and LP CAPs (>or= 25 microg/ml) differentially affected the endogenous scavengers, glutathione and nonprotein sulfhydryl in BV2 microglia after 1.5 h of exposure. Both HP and LP CAPs stimulated the release of proinflammatory cytokines tumor necrosis factor (TNF) alpha and interleukin (IL)-6 after 6 h of exposures. Microarray analysis of BV2 microglia exposed to either HP or LP CAPs (75 microg/ml, 4 h) identified 3200 (HP CAPs) and 160 (LP CAPs) differentially expressed (up- and downregulated) genes relative to media controls. Of the 3200 genes significantly affected by HP CAPs, the most prominent upregulated gene probes related to inflammatory pathways associated with Toll-like receptor signaling, MAPK signaling, T- and B-cell receptor signaling, apoptosis, and various proinflammatory cytokines and their receptors. LP CAPs significantly affected 160 genes that related to pathways associated with cellular maintenance and division, cell cycling and nuclear events. These data suggest that HP CAPs, which contained higher levels of nickel and vanadium than LP CAPs, appear to be more inflammatory and selectively upregulated the expression of inflammatory and innate immunity pathways in BV2 microglia.

    The cellular and genomic response of an immortalized microglia cell line (BV2) to concentrated ambient particulate matter. Publishing Authors By Initials

    p samaP Sama,tc longTC Long,s hesterS Hester,j tajubaJ Tajuba,j parkerJ Parker,lc chenLC Chen,b veronesiB Veronesi,

    For similar complex mixtures: particulate matter research abstracts see: complex mixtures: particulate matter research

    PUBMED ID PMID:

    MEDLINE DATE:

    The cellular and genomic response of an immortalized microglia cell line (BV2) to concentrated ambient particulate matter. Journal Published:

    PUBLICATION TYPE: Research Support, U.S. Gov't,

    Journal: Inhalation toxicology

    VOLUME: 19

    Page Numbers: 1079-87

    Journal Abbreviation:

    ISSN: 1091-7691

    DAY: 30

    MONTH: Oct

    YEAR: 2007

    The cellular and genomic response of an immortalized microglia cell line (BV2) to concentrated ambient particulate matter. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 8910739

    The cellular and genomic response of an immortalized microglia cell line (BV2) to concentrated ambient particulate matter. Keywords Mesh Terms:

    KEYWORDS: Particulate Matter

    MESH TERMS: toxicity

    Chemical & Substance for Abstract: The cellular and genomic response of an immortalized microglia cell line (BV2) to concentrated ambient particulate matter. Information

    Substance Name: Particulate Matter

    Registry Number: 0

    Grant and Affiliation Information for The cellular and genomic response of an immortalized microglia cell line (BV2) to concentrated ambient particulate matter.

    AFFILIATION: Department of Environmental Science and Engineering, University of North Carolina-Chapel Hill, Chapel Hill, North Carolina, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIEHS

    GRANT: R01ES015495

    ACRONYM: ES

    MEDLINETA: Inhal Toxicol

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

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