Aortic intimal resident macrophages are essential for maintenance of the non-thrombogenic intravascular state View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2022-01-12

AUTHORS

Gloria E. Hernandez, Feiyang Ma, Guadalupe Martinez, Nadia B. Firozabadi, Jocelynda Salvador, Lih Jiin Juang, Jerry Leung, Peng Zhao, Diego A. López, Reza Ardehali, Anna E. Beaudin, Christian J. Kastrup, Matteo Pellegrini, Matthew J. Flick, M. Luisa Iruela-Arispe

ABSTRACT

Leukocytes and endothelial cells frequently cooperate to resolve inflammatory events. In most cases, these interactions are transient in nature and triggered by immunological insults. Here, we report that, in areas of disturbed blood flow, aortic endothelial cells permanently and intimately associate with a population of specialized macrophages. These macrophages are recruited at birth from the closing ductus arteriosus and share the luminal surface with the endothelium, becoming interwoven in the tunica intima. Anatomical changes that affect hemodynamics, such as in patent ductus arteriosus, alter macrophage seeding to coincide with regions of disturbed flow. Aortic resident macrophages expand in situ via direct cell renewal. Induced depletion of intimal macrophages leads to thrombin-mediated endothelial cell contraction, progressive fibrin accumulation and formation of microthrombi that, once dislodged, cause blockade of vessels in several organs. Together the findings reveal that intravascular resident macrophages are essential to regulate thrombin activity and clear fibrin deposits in regions of disturbed blood flow. More... »

PAGES

67-84

References to SciGraph publications

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s44161-021-00006-4

    DOI

    http://dx.doi.org/10.1038/s44161-021-00006-4

    DIMENSIONS

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    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/35599984


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    19 schema:description Leukocytes and endothelial cells frequently cooperate to resolve inflammatory events. In most cases, these interactions are transient in nature and triggered by immunological insults. Here, we report that, in areas of disturbed blood flow, aortic endothelial cells permanently and intimately associate with a population of specialized macrophages. These macrophages are recruited at birth from the closing ductus arteriosus and share the luminal surface with the endothelium, becoming interwoven in the tunica intima. Anatomical changes that affect hemodynamics, such as in patent ductus arteriosus, alter macrophage seeding to coincide with regions of disturbed flow. Aortic resident macrophages expand in situ via direct cell renewal. Induced depletion of intimal macrophages leads to thrombin-mediated endothelial cell contraction, progressive fibrin accumulation and formation of microthrombi that, once dislodged, cause blockade of vessels in several organs. Together the findings reveal that intravascular resident macrophages are essential to regulate thrombin activity and clear fibrin deposits in regions of disturbed blood flow.
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    29 area
    30 arteriosus
    31 birth
    32 blockade
    33 blood flow
    34 cases
    35 cell contraction
    36 cell renewal
    37 cells
    38 changes
    39 contraction
    40 depletion
    41 deposits
    42 disturbed blood flow
    43 disturbed flow
    44 ductus arteriosus
    45 endothelial cell contraction
    46 endothelial cells
    47 endothelium
    48 events
    49 fibrin accumulation
    50 fibrin deposits
    51 findings
    52 flow
    53 formation
    54 formation of microthrombi
    55 hemodynamics
    56 immunological insults
    57 induced depletion
    58 inflammatory events
    59 insult
    60 interaction
    61 intima
    62 intimal macrophages
    63 leukocytes
    64 luminal surface
    65 macrophages
    66 maintenance
    67 microthrombi
    68 most cases
    69 nature
    70 organs
    71 patent ductus arteriosus
    72 population
    73 region
    74 renewal
    75 resident macrophages
    76 situ
    77 specialized macrophages
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