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    Area of Science:

    • Cardiovascular Biology
    • Regenerative Medicine
    • Molecular Biology

    Background:

    • Angiogenesis is crucial for healing ischemic injuries.
    • Cellular repressor of E1A-stimulated genes (CREG1) is known to affect endothelial cell (EC) behavior.
    • The role of CREG1 in angiogenesis was previously undefined.

    Purpose of the Study:

    • To investigate the role of CREG1 in promoting angiogenesis.
    • To elucidate the underlying mechanisms of CREG1-mediated angiogenesis.

    Main Methods:

    • Adenovirus-mediated CREG1 expression in human umbilical vein endothelial cells (HUVECs).
    • In vitro EC tube formation assays and in vivo matrigel plug assays in mice.
    • Analysis of filopodia formation, integrin-linked kinase (ILK), and Cdc42 activation.
    • Assessment of hindlimb perfusion in CREG1 heterozygous knockout mice and after CREG1 gene therapy.

    Main Results:

    • Adenovirus-transduced CREG1 increased HUVEC tube formation and neovascularization in vivo.
    • CREG1 enhanced filopodia formation, associated with increased ILK expression and Cdc42 activation.
    • CREG1 heterozygous knockout mice showed reduced hindlimb perfusion after ligation.
    • Intramuscular CREG1 gene therapy partially restored perfusion in ischemic hindlimbs.

    Conclusions:

    • CREG1 promotes angiogenesis by enhancing endothelial cell filopodia formation and vascular assembly through the ILK-Cdc42 pathway.
    • CREG1 represents a potential therapeutic target for ischemic vascular diseases.