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  1. Article ; Online: Redox regulation of endothelial canonical transient receptor potential channels.

    Cioffi, Donna L

    Antioxidants & redox signaling

    2011  Volume 15, Issue 6, Page(s) 1567–1582

    Abstract: The endothelium is a highly dynamic structure lining the inside of blood vessels that exhibits physical and chemical properties that are critical determinants of overall vascular function. Physically, the endothelium constitutes a semipermeable barrier. ... ...

    Abstract The endothelium is a highly dynamic structure lining the inside of blood vessels that exhibits physical and chemical properties that are critical determinants of overall vascular function. Physically, the endothelium constitutes a semipermeable barrier. Chemically, the endothelium synthesizes numerous factors such as reactive oxygen species (ROS) that can act as autocrine and paracrine signaling molecules. Oxidative stress results when ROS levels increase to levels that cause cellular injury, and, in the endothelium oxidative stress leads to barrier disruption. Endothelial barrier disruption also results from increased cytosolic calcium through store-operated calcium (SOC) entry channels. Although it is known that ROS can interact with and regulate some ion channels, relatively little is known about the interaction of these species with components of endothelial SOC entry channels, the canonical transient receptor potential (TRPC) proteins. Here we review our current understanding of ROS-mediated TRPC channel function and how it affects SOC entry and endothelial barrier disruption.
    MeSH term(s) Animals ; Blood Vessels/metabolism ; Calcium/chemistry ; Calcium/metabolism ; Cell Membrane/metabolism ; Endothelium, Vascular/metabolism ; Humans ; Muscle, Smooth, Vascular/metabolism ; NADPH Oxidases/metabolism ; Nitric Oxide/metabolism ; Oxidation-Reduction ; Reactive Oxygen Species/chemistry ; Reactive Oxygen Species/metabolism ; Signal Transduction ; Transient Receptor Potential Channels/chemistry ; Transient Receptor Potential Channels/metabolism ; Xanthine Oxidase/metabolism
    Chemical Substances Reactive Oxygen Species ; Transient Receptor Potential Channels ; Nitric Oxide (31C4KY9ESH) ; Xanthine Oxidase (EC 1.17.3.2) ; NADPH Oxidases (EC 1.6.3.-) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2011-05-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1483836-9
    ISSN 1557-7716 ; 1523-0864
    ISSN (online) 1557-7716
    ISSN 1523-0864
    DOI 10.1089/ars.2010.3740
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    Zs.A 5488: Show issues Location:
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  2. Article ; Online: Nuclear FAK in endothelium: An intrinsic inhibitor of NF-κB activation in atherosclerosis.

    Murphy, James M / Jeong, Kyuho / Tran, Duyen Thi Kieu / Cioffi, Donna L / Campbell, Pamela Moore / Kim, Jin H / Jo, Hanjoong / Ahn, Eun-Young Erin / Lim, Ssang-Taek Steve

    Atherosclerosis

    2023  Volume 379, Page(s) 117189

    Abstract: Background and aims: Hyperlipidemia leads to the accumulation of oxidized low-density lipoprotein (oxLDL) within the vessel wall where it causes chronic inflammation in endothelial cells (ECs) and drives atherosclerotic lesions. Although focal adhesion ... ...

    Abstract Background and aims: Hyperlipidemia leads to the accumulation of oxidized low-density lipoprotein (oxLDL) within the vessel wall where it causes chronic inflammation in endothelial cells (ECs) and drives atherosclerotic lesions. Although focal adhesion kinase (FAK) is critical in proinflammatory NF-κB activation in ECs, it is unknown if hyperlipidemia alters FAK-mediated NF-κB activity in vivo to affect atherosclerosis progression.
    Methods: We investigated changes in EC FAK and NF-κB activation using Apoe
    Results: ECs of hyperlipidemic mice clearly showed much higher levels of FAK activation in the cytoplasm, which was associated with increased NF-κB activation compared to normal diet (ND) group. On the contrary, FAK is mostly localized in the nucleus and inactive in ECs under healthy conditions with a low NF-κB activity. Both pharmacological and EC-specific genetic FAK inhibition in WD fed Apoe
    Conclusions: Hyperlipidemic conditions activate NF-κB pathway by increasing EC FAK activity and cytoplasmic localization in mice and human atherosclerotic samples. As FAK inhibition can efficiently reduce vascular inflammation and atherosclerotic lesions in mice by reversing EC FAK localization and NF-κB activation, these findings support a potential use for FAK inhibitors in treating atherosclerosis.
    MeSH term(s) Animals ; Humans ; Mice ; Apolipoproteins E/genetics ; Apolipoproteins E/metabolism ; Atherosclerosis/genetics ; Endothelial Cells/metabolism ; Endothelium ; Focal Adhesion Protein-Tyrosine Kinases/metabolism ; Hyperlipidemias/complications ; Inflammation/metabolism ; NF-kappa B/metabolism
    Chemical Substances Apolipoproteins E ; Focal Adhesion Protein-Tyrosine Kinases (EC 2.7.10.2) ; NF-kappa B
    Language English
    Publishing date 2023-07-26
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80061-2
    ISSN 1879-1484 ; 0021-9150
    ISSN (online) 1879-1484
    ISSN 0021-9150
    DOI 10.1016/j.atherosclerosis.2023.117189
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  3. Article ; Online: The skinny on TRPV1.

    Cioffi, Donna L

    Circulation research

    2007  Volume 100, Issue 7, Page(s) 934–936

    MeSH term(s) Adipogenesis ; Capsaicin/pharmacology ; Humans ; Obesity/prevention & control ; TRPV Cation Channels/metabolism
    Chemical Substances TRPV Cation Channels ; TRPV1 protein, human ; TRPV1 protein, mouse ; Capsaicin (S07O44R1ZM)
    Language English
    Publishing date 2007-04-13
    Publishing country United States
    Document type Comment ; Editorial ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/01.RES.0000265139.10277.62
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  4. Article ; Online: Feedback regulation of cone cyclic nucleotide channels by phosphoinositides. Focus on "CNGA3 achromatopsia-associated mutation potentiates the phosphoinositide sensitivity of cone photoreceptor CNG channels by altering intersubunit interactions".

    Cioffi, Donna L / Rich, Thomas C

    American journal of physiology. Cell physiology

    2013  Volume 305, Issue 2, Page(s) C131–2

    MeSH term(s) Animals ; Color Vision Defects/genetics ; Cyclic Nucleotide-Gated Cation Channels/metabolism ; Gene Expression Regulation/physiology ; Humans ; Phosphatidylinositols/pharmacology ; Protein Subunits ; Retinal Cone Photoreceptor Cells/drug effects
    Chemical Substances CNGA3 protein, human ; Cyclic Nucleotide-Gated Cation Channels ; Phosphatidylinositols ; Protein Subunits
    Language English
    Publishing date 2013-05-15
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00136.2013
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  5. Article ; Online: Focal Adhesion Kinase Activity and Localization is Critical for TNF-α-Induced Nuclear Factor-κB Activation.

    Murphy, James M / Jeong, Kyuho / Cioffi, Donna L / Campbell, Pamela Moore / Jo, Hanjoong / Ahn, Eun-Young Erin / Lim, Ssang-Taek Steve

    Inflammation

    2021  Volume 44, Issue 3, Page(s) 1130–1144

    Abstract: While sustained nuclear factor-κB (NF-κB) activation is critical for proinflammatory molecule expression, regulators of NF-κB activity during chronic inflammation are not known. We investigated the role of focal adhesion kinase (FAK) on sustained NF-κB ... ...

    Abstract While sustained nuclear factor-κB (NF-κB) activation is critical for proinflammatory molecule expression, regulators of NF-κB activity during chronic inflammation are not known. We investigated the role of focal adhesion kinase (FAK) on sustained NF-κB activation in tumor necrosis factor-α (TNF-α)-stimulated endothelial cells (ECs) both in vitro and in vivo. We found that FAK inhibition abolished TNF-α-mediated sustained NF-κB activity in ECs by disrupting formation of TNF-α receptor complex-I (TNFRC-I). Additionally, FAK inhibition diminished recruitment of receptor-interacting serine/threonine-protein kinase 1 (RIPK1) and the inhibitor of NF-κB (IκB) kinase (IKK) complex to TNFRC-I, resulting in elevated stability of IκBα protein. In mice given TNF-α, pharmacological and genetic FAK inhibition blocked TNF-α-induced IKK-NF-κB activation in aortic ECs. Mechanistically, TNF-α activated and redistributed FAK from the nucleus to the cytoplasm, causing elevated IKK-NF-κB activation. On the other hand, FAK inhibition trapped FAK in the nucleus of ECs even upon TNF-α stimulation, leading to reduced IKK-NF-κB activity. Together, these findings support a potential use for FAK inhibitors in treating chronic inflammatory diseases.
    MeSH term(s) Active Transport, Cell Nucleus ; Animals ; Cells, Cultured ; Focal Adhesion Kinase 1/genetics ; Focal Adhesion Kinase 1/metabolism ; Human Umbilical Vein Endothelial Cells/drug effects ; Human Umbilical Vein Endothelial Cells/enzymology ; Human Umbilical Vein Endothelial Cells/immunology ; Humans ; I-kappa B Kinase/metabolism ; Inflammation/enzymology ; Inflammation/immunology ; Mice, Inbred C57BL ; Mice, Knockout ; NF-KappaB Inhibitor alpha/metabolism ; NF-kappa B/metabolism ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; Signal Transduction ; Tumor Necrosis Factor-alpha/pharmacology ; Mice
    Chemical Substances NF-kappa B ; TNF protein, human ; Tumor Necrosis Factor-alpha ; NF-KappaB Inhibitor alpha (139874-52-5) ; Focal Adhesion Kinase 1 (EC 2.7.10.2) ; PTK2 protein, human (EC 2.7.10.2) ; Ptk2 protein, mouse (EC 2.7.10.2) ; RIPK1 protein, human (EC 2.7.11.1) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Ripk1 protein, mouse (EC 2.7.11.1) ; I-kappa B Kinase (EC 2.7.11.10)
    Language English
    Publishing date 2021-02-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 434408-x
    ISSN 1573-2576 ; 0360-3997
    ISSN (online) 1573-2576
    ISSN 0360-3997
    DOI 10.1007/s10753-020-01408-5
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  6. Article ; Online: S100A6 is a positive regulator of PPP5C-FKBP51-dependent regulation of endothelial calcium signaling.

    Haldar, Barnita / Hamilton, Caleb L / Solodushko, Viktoriya / Abney, Kevin A / Alexeyev, Mikhail / Honkanen, Richard E / Scammell, Jonathan G / Cioffi, Donna L

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2020  Volume 34, Issue 2, Page(s) 3179–3196

    Abstract: ... ...

    Abstract I
    MeSH term(s) Animals ; Calcium Signaling ; Cell Cycle Proteins/metabolism ; Cells, Cultured ; Endothelial Cells/metabolism ; Endothelium, Vascular/cytology ; Lung/blood supply ; Nuclear Proteins/metabolism ; Phosphoprotein Phosphatases/metabolism ; Protein Binding ; Protein Transport ; Rats ; S100 Calcium Binding Protein A6/metabolism ; TRPC Cation Channels/metabolism ; Tacrolimus Binding Proteins/metabolism
    Chemical Substances Cell Cycle Proteins ; Nuclear Proteins ; S100 Calcium Binding Protein A6 ; S100a6 protein, rat ; TRPC Cation Channels ; TRPC4 ion channel ; Phosphoprotein Phosphatases (EC 3.1.3.16) ; protein phosphatase 5 (EC 3.1.3.16) ; Tacrolimus Binding Proteins (EC 5.2.1.-) ; tacrolimus binding protein 5 (EC 5.2.1.8)
    Language English
    Publishing date 2020-01-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.201901777R
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  7. Article ; Online: Lectin-Based Characterization of Vascular Cell Microparticle Glycocalyx.

    Scruggs, April K / Cioffi, Eugene A / Cioffi, Donna L / King, Judy A C / Bauer, Natalie N

    PloS one

    2015  Volume 10, Issue 8, Page(s) e0135533

    Abstract: Microparticles (MPs) are released constitutively and from activated cells. MPs play significant roles in vascular homeostasis, injury, and as biomarkers. The unique glycocalyx on the membrane of cells has frequently been exploited to identify specific ... ...

    Abstract Microparticles (MPs) are released constitutively and from activated cells. MPs play significant roles in vascular homeostasis, injury, and as biomarkers. The unique glycocalyx on the membrane of cells has frequently been exploited to identify specific cell types, however the glycocalyx of the MPs has yet to be defined. Thus, we sought to determine whether MPs, released both constitutively and during injury, from vascular cells have a glycocalyx matching those of the parental cell type to provide information on MP origin. For these studies we used rat pulmonary microvascular and artery endothelium, pulmonary smooth muscle, and aortic endothelial cells. MPs were collected from healthy or cigarette smoke injured cells and analyzed with a panel of lectins for specific glycocalyx linkages. Intriguingly, we determined that the MPs released either constitutively or stimulated by CSE injury did not express the same glycocalyx of the parent cells. Further, the glycocalyx was not unique to any of the specific cell types studied. These data suggest that MPs from both normal and healthy vascular cells do not share the parental cell glycocalyx makeup.
    MeSH term(s) Animals ; Cell-Derived Microparticles/chemistry ; Cell-Derived Microparticles/drug effects ; Cell-Derived Microparticles/metabolism ; Cells, Cultured ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Endothelium, Vascular/cytology ; Glycocalyx/chemistry ; Glycocalyx/drug effects ; Glycocalyx/metabolism ; Lectins/metabolism ; Microscopy, Electron, Transmission ; Rats ; Smoking/adverse effects
    Chemical Substances Lectins
    Language English
    Publishing date 2015
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0135533
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  8. Article ; Online: Terminal sialic acids are an important determinant of pulmonary endothelial barrier integrity.

    Cioffi, Donna L / Pandey, Subha / Alvarez, Diego F / Cioffi, Eugene A

    American journal of physiology. Lung cellular and molecular physiology

    2012  Volume 302, Issue 10, Page(s) L1067–77

    Abstract: The surface of vascular endothelium bears a glycocalyx comprised, in part, of a complex mixture of oligosaccharide chains attached to cell-surface proteins and membrane lipids. Importantly, understanding of the structure and function of the endothelial ... ...

    Abstract The surface of vascular endothelium bears a glycocalyx comprised, in part, of a complex mixture of oligosaccharide chains attached to cell-surface proteins and membrane lipids. Importantly, understanding of the structure and function of the endothelial glycocalyx is poorly understood. Preliminary studies have demonstrated structural differences in the glycocalyx of pulmonary artery endothelial cells compared with pulmonary microvascular endothelial cells. Herein we begin to probe in more detail structural and functional attributes of endothelial cell-surface carbohydrates. In this study we focus on the expression and function of sialic acids in pulmonary endothelium. We observed that, although pulmonary microvascular endothelial cells express similar amounts of total sialic acids as pulmonary artery endothelial cells, the nature of the sialic acid linkages differs between the two cell types such that pulmonary artery endothelial cells express both α(2,3)- and α(2,6)-linked sialic acids on the surface (i.e., surficially), whereas microvascular endothelial cells principally express α(2,3)-linked sialic acids. To determine whether sialic acids play a role in endothelial barrier function, cells were treated with neuraminidases to hydrolyze sialic acid moieties. Disruption of cell-cell and cell-matrix adhesions was observed following neuraminidase treatment, suggesting that terminal sialic acids promote endothelial barrier integrity. When we measured transendothelial resistance, differential responses of pulmonary artery and microvascular endothelial cells to neuraminidase from Clostridium perfringens suggest that the molecular architecture of the sialic acid glycomes differs between these two cell types. Collectively our observations reveal critical structural and functional differences of terminally linked sialic acids on the pulmonary endothelium.
    MeSH term(s) Animals ; Capillaries/chemistry ; Capillaries/cytology ; Capillaries/metabolism ; Capillary Permeability ; Cell-Matrix Junctions/chemistry ; Cell-Matrix Junctions/drug effects ; Cell-Matrix Junctions/physiology ; Cells, Cultured ; Clostridium perfringens ; Electric Impedance ; Endothelial Cells/chemistry ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Endothelium, Vascular/chemistry ; Endothelium, Vascular/cytology ; Endothelium, Vascular/metabolism ; Glycocalyx/chemistry ; Glycocalyx/physiology ; Neuraminidase/metabolism ; Neuraminidase/pharmacology ; Organ Specificity ; Pulmonary Artery/chemistry ; Pulmonary Artery/cytology ; Pulmonary Artery/metabolism ; Rats ; Sialic Acids/chemistry ; Sialic Acids/physiology
    Chemical Substances Sialic Acids ; Neuraminidase (EC 3.2.1.18)
    Language English
    Publishing date 2012-03-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1013184-x
    ISSN 1522-1504 ; 1040-0605
    ISSN (online) 1522-1504
    ISSN 1040-0605
    DOI 10.1152/ajplung.00190.2011
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  9. Article ; Online: Studies on the resolution of subcellular free calcium concentrations: a technological advance. Focus on "detection of differentially regulated subsarcolemmal calcium signals activated by vasoactive agonists in rat pulmonary artery smooth muscle cells".

    Xu, Ningyong / Francis, Michael / Cioffi, Donna L / Stevens, Troy

    American journal of physiology. Cell physiology

    2014  Volume 306, Issue 7, Page(s) C636–8

    MeSH term(s) Animals ; Calcium Signaling/drug effects ; Male ; Muscle, Smooth, Vascular/drug effects ; Myocytes, Smooth Muscle/drug effects ; Sarcolemma/drug effects ; Vasoconstriction/drug effects ; Vasoconstrictor Agents/pharmacology
    Chemical Substances Vasoconstrictor Agents
    Language English
    Publishing date 2014-02-19
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00046.2014
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  10. Article: Protective role of FKBP51 in calcium entry-induced endothelial barrier disruption.

    Hamilton, Caleb L / Kadeba, Pierre I / Vasauskas, Audrey A / Solodushko, Viktoriya / McClinton, Anna K / Alexeyev, Mikhail / Scammell, Jonathan G / Cioffi, Donna L

    Pulmonary circulation

    2017  Volume 8, Issue 1, Page(s) 2045893217749987

    Abstract: Pulmonary artery endothelial cells (PAECs) express a cation current, ... ...

    Abstract Pulmonary artery endothelial cells (PAECs) express a cation current, I
    Language English
    Publishing date 2017-12-20
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2638089-4
    ISSN 2045-8940 ; 2045-8932
    ISSN (online) 2045-8940
    ISSN 2045-8932
    DOI 10.1177/2045893217749987
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