Human vascular endothelial cells, granulopoiesis, and the inflammatory response

Grover C. Bagby, Gray Shaw, Gerald M. Segal

    Research output: Contribution to journalArticle

    11 Citations (Scopus)

    Abstract

    We have carried out a series of in vitro studies designed to characterize the role of mononuclear phagocytes as regulators of hematopoiesis. The results of these studies have demonstrated that mononuclear phagocytes produce factors, including interleukin-1 (IL-1), that induce the expression of multilineage hematopoietic growth factors by human vascular endothelial cells. In more recent studies we and others have identified these induced factors as G-CSF, GM-CSF, IL-6, and IL-1. Interleukin 1 stimulates expression of these genes by inducing the accumulation of gene transcripts. Moreover, transcript accumulation, at least with GM-CSF, results from prolongation of mRNA half-life. Based on preliminary studies in a cell-free system, we propose that the inductive capacity of IL-1 results from its activation of ribonuclease inhibitors in the cytoplasm of IL-1-induced cells and hypothesize that this may be a general mechanism by which IL-1 induces gene expression.

    Original languageEnglish (US)
    JournalJournal of Investigative Dermatology
    Volume93
    Issue number2 SUPPL.
    StatePublished - Aug 1989

    Fingerprint

    Endothelial cells
    Interleukin-1
    Endothelial Cells
    Granulocyte-Macrophage Colony-Stimulating Factor
    Phagocytes
    Genes
    Gene Expression
    Cell-Free System
    Hematopoiesis
    Granulocyte Colony-Stimulating Factor
    Ribonucleases
    Gene expression
    Half-Life
    Interleukin-6
    Intercellular Signaling Peptides and Proteins
    Cytoplasm
    Chemical activation
    Messenger RNA

    ASJC Scopus subject areas

    • Dermatology

    Cite this

    Human vascular endothelial cells, granulopoiesis, and the inflammatory response. / Bagby, Grover C.; Shaw, Gray; Segal, Gerald M.

    In: Journal of Investigative Dermatology, Vol. 93, No. 2 SUPPL., 08.1989.

    Research output: Contribution to journalArticle

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