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  1. Artikel ; Online: Differential Production of Midkine and Pleiotrophin by Innate APCs upon Stimulation through Nucleic Acid-Sensing TLRs.

    Said, Elias A / Al-Dughaishi, Sumaya / Al-Hatmi, Wadha / Al-Reesi, Iman / Al-Balushi, Mohammed S / Al-Bimani, Atika / Al-Busaidi, Juma Z / Al-Riyami, Marwa / Al-Khabori, Murtadha / Al-Kindi, Salam / Procopio, Francesco A / Al-Sinawi, Shadia / Al-Ansari, Aliyaa / Koh, Crystal Y / Al-Naamani, Khalid / Al-Jabri, Ali A

    Journal of immunology research

    2023  Band 2023, Seite(n) 7944102

    Abstract: Midkine (MK) and pleiotrophin (PTN) belong to the same family of cytokines. They have similar sequences and functions. Both have important roles in cellular proliferation, tumors, and diseases. They regulate and are expressed by some immune cells. We ... ...

    Abstract Midkine (MK) and pleiotrophin (PTN) belong to the same family of cytokines. They have similar sequences and functions. Both have important roles in cellular proliferation, tumors, and diseases. They regulate and are expressed by some immune cells. We have recently demonstrated MK production by some human innate antigen-presenting cells (iAPCs), i.e., monocyte-derived dendritic cells (MDDCs) and macrophages stimulated through Toll-like receptor (TLR)-4, and plasmacytoid dendritic cells (pDCs) stimulated through TLR 7. While PTN production was only documented in tissue macrophages. TLRs 3, 7, 8, and 9 are nucleic acid sensing (NAS) TLRs that detect nucleic acids from cell damage and infection and induce iAPC responses. We investigated whether NAS TLRs can induce MK and PTN production by human iAPCs, namely monocytes, macrophages, MDDCs, myeloid dendritic cells (mDCs), and pDCs. Our results demonstrated for the first time that PTN is produced by all iAPCs upon TLR triggering (
    Mesh-Begriff(e) Humans ; Cytokines ; Dendritic Cells ; Midkine ; Neoplasms
    Chemische Substanzen Cytokines ; Midkine (137497-38-2) ; pleiotrophin (134034-50-7) ; MDK protein, human
    Sprache Englisch
    Erscheinungsdatum 2023-10-09
    Erscheinungsland Egypt
    Dokumenttyp Journal Article
    ZDB-ID 2817541-4
    ISSN 2314-7156 ; 2314-7156
    ISSN (online) 2314-7156
    ISSN 2314-7156
    DOI 10.1155/2023/7944102
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Human macrophages and monocyte-derived dendritic cells stimulate the proliferation of endothelial cells through midkine production.

    Said, Elias A / Al-Dughaishi, Sumaya / Al-Hatmi, Wadha / Al-Reesi, Iman / Al-Riyami, Marwa / Al-Balushi, Mohammed S / Al-Bimani, Atika / Al-Busaidi, Juma Z / Al-Khabori, Murtadha / Al-Kindi, Salam / Procopio, Francesco A / Al-Rashdi, Afrah / Al-Ansari, Aliyaa / Babiker, Hamza / Koh, Crystal Y / Al-Naamani, Khalid / Pantaleo, Giuseppe / Al-Jabri, Ali A

    PloS one

    2022  Band 17, Heft 4, Seite(n) e0267662

    Abstract: The cytokine midkine (MK) is a growth factor that is involved in different physiological processes including tissue repair, inflammation, the development of different types of cancer and the proliferation of endothelial cells. The production of MK by ... ...

    Abstract The cytokine midkine (MK) is a growth factor that is involved in different physiological processes including tissue repair, inflammation, the development of different types of cancer and the proliferation of endothelial cells. The production of MK by primary human macrophages and monocyte-derived dendritic cells (MDDCs) was never described. We investigated whether MK is produced by primary human monocytes, macrophages and MDDCs and the capacity of macrophages and MDDCs to modulate the proliferation of endothelial cells through MK production. The TLR stimulation of human monocytes, macrophages and MDDCs induced an average of ≈200-fold increase in MK mRNA and the production of an average of 78.2, 62, 179 pg/ml MK by monocytes, macrophages and MDDCs respectively (p < 0.05). MK production was supported by its detection in CD11c+ cells, CLEC4C+ cells and CD68+ cells in biopsies of human tonsils showing reactive lymphoid follicular hyperplasia. JSH-23, which selectively inhibits NF-κB activity, decreased the TLR-induced production of MK in PMBCs, macrophages and MDDCs compared to the control (p < 0.05). The inhibition of MK production by macrophages and MDDCs using anti-MK siRNA decreased the capacity of their supernatants to stimulate the proliferation of endothelial cells (p = 0.01 and 0.04 respectively). This is the first study demonstrating that the cytokine MK is produced by primary human macrophages and MDDCs upon TLR triggering, and that these cells can stimulate endothelial cell proliferation through MK production. Our results also suggest that NF-κB plays a potential role in the production of MK in macrophages and MDDCs upon TLR stimulation. The production of MK by macrophages and MDDCs and the fact that these cells can enhance the proliferation of endothelial cells by producing MK are novel immunological phenomena that have potentially important therapeutic implications.
    Mesh-Begriff(e) Cell Proliferation ; Cytokines/metabolism ; Dendritic Cells ; Endothelial Cells ; Humans ; Lectins, C-Type/metabolism ; Macrophages ; Membrane Glycoproteins/metabolism ; Midkine/metabolism ; Monocytes ; NF-kappa B/metabolism ; Receptors, Immunologic/metabolism
    Chemische Substanzen CLEC4C protein, human ; Cytokines ; Lectins, C-Type ; Membrane Glycoproteins ; NF-kappa B ; Receptors, Immunologic ; Midkine (137497-38-2)
    Sprache Englisch
    Erscheinungsdatum 2022-04-27
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0267662
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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