Cytoglobin Expression Is Induced in Vascular Smooth Muscle Cells Through Endothelial Cell-Derived Notch Signaling: Implications of a Protective Role in Blood Vessel Function
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Series/Report no.:2017 Fall Undergraduate Research Student Poster Forum. 11th
Communication between endothelial cells and smooth muscle cells is required for normal blood vessel formation and function. My research focuses on understanding the molecular signaling pathways that govern cell-cell communication and maintain vascular function. The Notch signaling pathway is an established mediator in cell-cell communication. Notch signaling is activated in smooth muscle cells by adjacent endothelial cells and induces gene expression profiles that determine smooth muscle cell function. In this study, I identified Cytoglobin as a gene that is induced in smooth muscle cells by co-cultured endothelial cells. Cytoglobin is a hexa-coordinate hemoglobin that has been implicated in stress regulation through its modulation of nitric oxide and reactive oxygen species. My data demonstrate that Cytoglobin is induced in smooth muscle cells via the Notch signaling pathway and that smooth-muscle expressed Notch receptors are both necessary and sufficient for Cytoglobin expression. Cytoglobin induction by endothelial-derived Notch signaling is altered when smooth muscle cells are cultured with nitric oxide modulators, hypoxia mimics, and reactive oxygen species. This alteration hints at Cytoglobin’s potential role in modulating redox stress. My findings thus far support the notion that endothelial cells induce Cytoglobin expression in smooth muscle cells as a means to regulate nitric oxide bioavailability in blood vessels. Further examination of Notch signaling and Cytoglobin expression in dysfunctional vessels may reveal novel targets for therapeutic intervention of vascular-associated diseases.
Academic Major: Chemistry
Nationwide Children’s Hospital
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