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  1. Article ; Online: Vascular Inflammation and Smooth Muscle Contractility: The Role of Nox1-Derived Superoxide and LRRC8 Anion Channels.

    Lamb, Fred S / Choi, Hyehun / Miller, Michael R / Stark, Ryan J

    Hypertension (Dallas, Tex. : 1979)

    2024  Volume 81, Issue 4, Page(s) 752–763

    Abstract: Vascular inflammation underlies the development of hypertension, and the mechanisms by which it increases blood pressure remain the topic of intense investigation. Proinflammatory factors including glucose, salt, vasoconstrictors, cytokines, wall stress, ...

    Abstract Vascular inflammation underlies the development of hypertension, and the mechanisms by which it increases blood pressure remain the topic of intense investigation. Proinflammatory factors including glucose, salt, vasoconstrictors, cytokines, wall stress, and growth factors enhance contractility and impair relaxation of vascular smooth muscle cells. These pathways share a dependence upon redox signaling, and excessive activation promotes oxidative stress that promotes vascular aging. Vascular smooth muscle cell phenotypic switching and migration into the intima contribute to atherosclerosis, while hypercontractility increases systemic vascular resistance and vasospasm that can trigger ischemia. Here, we review factors that drive the initiation and progression of this vasculopathy in vascular smooth muscle cells. Emphasis is placed on the contribution of reactive oxygen species generated by the Nox1 NADPH oxidase which produces extracellular superoxide (O
    MeSH term(s) Humans ; Superoxides/metabolism ; Muscle, Smooth, Vascular/metabolism ; NADPH Oxidase 1/metabolism ; NADPH Oxidases/metabolism ; Reactive Oxygen Species/metabolism ; Hypertension/metabolism ; Myocytes, Smooth Muscle/metabolism ; Cells, Cultured
    Chemical Substances Superoxides (11062-77-4) ; NADPH Oxidase 1 (EC 1.6.3.-) ; NADPH Oxidases (EC 1.6.3.-) ; Reactive Oxygen Species
    Language English
    Publishing date 2024-01-04
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.123.19434
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1488: Show issues Location:
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  2. Article: Localising oxidant "stress" in the antiphospholipid syndrome.

    Lamb, Fred S

    Thrombosis and haemostasis

    2015  Volume 113, Issue 5, Page(s) 915

    MeSH term(s) Animals ; Antiphospholipid Syndrome/immunology ; Carrier Proteins/metabolism ; Endosomes/metabolism ; Female ; Humans ; Male ; NADPH Oxidases/metabolism
    Chemical Substances Carrier Proteins ; NADPH Oxidases (EC 1.6.3.-)
    Language English
    Publishing date 2015-05
    Publishing country Germany
    Document type Journal Article ; Comment
    ZDB-ID 518294-3
    ISSN 0340-6245
    ISSN 0340-6245
    DOI 10.1160/TH15-03-0218
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  3. Article ; Online: The Inverse Relationship Between Endothelium-Dependent Vasodilation and Blood Pressure is Lost After Cardiopulmonary Bypass.

    Stark, Ryan J / Krispinsky, Luke T / Lamb, Fred S

    Journal of cardiovascular translational research

    2021  Volume 14, Issue 6, Page(s) 1114–1116

    Abstract: Cardiopulmonary bypass (CPB) is required for the surgical correction of congenital heart defects and incites an acute inflammatory response that impairs endothelial function post-operatively. Therefore, we hypothesized that the pre-operative relationship ...

    Abstract Cardiopulmonary bypass (CPB) is required for the surgical correction of congenital heart defects and incites an acute inflammatory response that impairs endothelial function post-operatively. Therefore, we hypothesized that the pre-operative relationship between endothelial function and blood pressure would be impaired after CPB-mediated inflammation. Using laser Doppler perfusion monitoring coupled with iontophoresis, we found that while there was a significant inverse correlation between endothelium-dependent vascular reactivity to acetylcholine (ACh) stimulation and systolic blood pressure (SBP), this relationship was lost after CPB. No relationship was observed between endothelium-independent vascular reactivity using sodium nitroprusside (SNP) and SBP either pre-CPB or any point thereafter. Additionally, neither CPB time nor inflammatory cytokines correlated with the degree of responsiveness to ACh. These data suggest that the measurement of endothelium impairment after CPB may be more reflective of cardiovascular health than SBP alone.
    MeSH term(s) Acetylcholine/pharmacology ; Blood Pressure/drug effects ; Cardiopulmonary Bypass ; Endothelium, Vascular/physiopathology ; Female ; Heart Defects, Congenital/surgery ; Humans ; Infant ; Iontophoresis ; Laser-Doppler Flowmetry ; Male ; Nitroprusside/pharmacology ; Vasodilation/drug effects ; Vasodilator Agents/pharmacology
    Chemical Substances Vasodilator Agents ; Nitroprusside (169D1260KM) ; Acetylcholine (N9YNS0M02X)
    Language English
    Publishing date 2021-04-09
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2422411-X
    ISSN 1937-5395 ; 1937-5387
    ISSN (online) 1937-5395
    ISSN 1937-5387
    DOI 10.1007/s12265-021-10124-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Extracellular SOD modulates canonical TNFα signaling and α5β1 integrin transactivation in vascular smooth muscle cells.

    Choi, Hyehun / Miller, Michael R / Nguyen, Hong-Ngan / Surratt, Victoria E / Koch, Stephen R / Stark, Ryan J / Lamb, Fred S

    Free radical biology & medicine

    2023  Volume 209, Issue Pt 1, Page(s) 152–164

    Abstract: TNFα activates NADPH oxidase 1 (Nox1) in vascular smooth muscle cells (VSMCs). The extracellular superoxide anion ( ... ...

    Abstract TNFα activates NADPH oxidase 1 (Nox1) in vascular smooth muscle cells (VSMCs). The extracellular superoxide anion (O
    MeSH term(s) Mice ; Animals ; Muscle, Smooth, Vascular/metabolism ; Tumor Necrosis Factor-alpha/genetics ; Superoxide Dismutase/metabolism ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Hydrogen Peroxide/metabolism ; Transcriptional Activation ; Signal Transduction ; Integrins/genetics ; Integrins/metabolism
    Chemical Substances Tumor Necrosis Factor-alpha ; Superoxide Dismutase (EC 1.15.1.1) ; NF-kappa B ; Hydrogen Peroxide (BBX060AN9V) ; Integrins
    Language English
    Publishing date 2023-10-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 807032-5
    ISSN 1873-4596 ; 0891-5849
    ISSN (online) 1873-4596
    ISSN 0891-5849
    DOI 10.1016/j.freeradbiomed.2023.10.397
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2109: Show issues Location:
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  5. Article ; Online: Neuronal ASIC1A As a Cerebral pH Sensor: Bringing the Flow.

    Stark, Ryan J / Choi, Hyehun / Lamb, Fred S

    Circulation research

    2019  Volume 125, Issue 10, Page(s) 921–923

    MeSH term(s) Acid Sensing Ion Channels ; Hydrogen-Ion Concentration ; Neurons
    Chemical Substances Acid Sensing Ion Channels
    Language English
    Publishing date 2019-10-24
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.119.315925
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Chloride Channel-3 (ClC-3) Modifies the Trafficking of Leucine-Rich Repeat-Containing 8A (LRRC8A) Anion Channels.

    Stark, Ryan J / Nguyen, Hong N / Bacon, Matthew K / Rohrbough, Jeffrey C / Choi, Hyehun / Lamb, Fred S

    The Journal of membrane biology

    2022  Volume 256, Issue 2, Page(s) 125–135

    Abstract: Chloride channel-3 (ClC-3) ... ...

    Abstract Chloride channel-3 (ClC-3) Cl
    MeSH term(s) Humans ; Membrane Proteins/metabolism ; Leucine ; HEK293 Cells ; Chloride Channels/genetics ; Chloride Channels/metabolism ; Anions/metabolism
    Chemical Substances Membrane Proteins ; Leucine (GMW67QNF9C) ; Chloride Channels ; Anions ; LRRC8A protein, human
    Language English
    Publishing date 2022-11-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 3082-x
    ISSN 1432-1424 ; 0022-2631
    ISSN (online) 1432-1424
    ISSN 0022-2631
    DOI 10.1007/s00232-022-00271-9
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    Zs.A 613: Show issues Location:
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  7. Article ; Online: Oxidant-resistant LRRC8A/C anion channels support superoxide production by NADPH oxidase 1.

    Choi, Hyehun / Rohrbough, Jeffrey C / Nguyen, Hong N / Dikalova, Anna / Lamb, Fred S

    The Journal of physiology

    2021  Volume 599, Issue 12, Page(s) 3013–3036

    Abstract: Key points: LRRC8A-containing anion channels associate with NADPH oxidase 1 (Nox1) and regulate superoxide production and tumour necrosis factor-α (TNFα) signalling. Here we show that LRRC8C and 8D also co-immunoprecipitate with Nox1 in vascular smooth ... ...

    Abstract Key points: LRRC8A-containing anion channels associate with NADPH oxidase 1 (Nox1) and regulate superoxide production and tumour necrosis factor-α (TNFα) signalling. Here we show that LRRC8C and 8D also co-immunoprecipitate with Nox1 in vascular smooth muscle cells. LRRC8C knockdown inhibited TNFα-induced O
    Abstract: Tumour necrosis factor-α (TNFα) activates NADPH oxidase 1 (Nox1) in vascular smooth muscle cells (VSMCs), producing superoxide (O
    MeSH term(s) Anions ; HEK293 Cells ; Humans ; Membrane Proteins ; NADPH Oxidase 1 ; Oxidants ; Superoxides
    Chemical Substances Anions ; LRRC8A protein, human ; Membrane Proteins ; Oxidants ; Superoxides (11062-77-4) ; NADPH Oxidase 1 (EC 1.6.3.-)
    Language English
    Publishing date 2021-05-26
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3115-x
    ISSN 1469-7793 ; 0022-3751
    ISSN (online) 1469-7793
    ISSN 0022-3751
    DOI 10.1113/JP281577
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Localising oxidant “stress” in the antiphospholipid syndrome

    S. Lamb, Fred

    Thrombosis and Haemostasis

    2015  Volume 113, Issue 05, Page(s) 915–915

    Language English
    Publishing date 2015-09-01
    Publisher Schattauer GmbH
    Publishing place Stuttgart ; New York
    Document type Article
    ZDB-ID 518294-3
    ISSN 2567-689X ; 0340-6245
    ISSN (online) 2567-689X
    ISSN 0340-6245
    DOI 10.1160/TH15-03-0218
    Database Thieme publisher's database

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  9. Article ; Online: TNFα and Reactive Oxygen Signaling in Vascular Smooth Muscle Cells in Hypertension and Atherosclerosis.

    Lamb, Fred S / Choi, Hyehun / Miller, Michael R / Stark, Ryan J

    American journal of hypertension

    2020  Volume 33, Issue 10, Page(s) 902–913

    Abstract: Hypertension and atherosclerosis, the predecessors of stroke and myocardial infarction, are chronic vascular inflammatory reactions. Tumor necrosis factor alpha (TNFα), the "master" proinflammatory cytokine, contributes to both the initiation and ... ...

    Abstract Hypertension and atherosclerosis, the predecessors of stroke and myocardial infarction, are chronic vascular inflammatory reactions. Tumor necrosis factor alpha (TNFα), the "master" proinflammatory cytokine, contributes to both the initiation and maintenance of vascular inflammation. TNFα induces reactive oxygen species (ROS) production which drives the redox reactions that constitute "ROS signaling." However, these ROS may also cause oxidative stress which contributes to vascular dysfunction. Mice lacking TNFα or its receptors are protected against both acute and chronic cardiovascular injury. Humans suffering from TNFα-driven inflammatory conditions such as rheumatoid arthritis and psoriasis are at increased cardiovascular risk. When treated with highly specific biologic agents that target TNFα signaling (Etanercept, etc.) they display marked reductions in that risk. The ability of TNFα to induce endothelial dysfunction, often the first step in a progression toward serious vasculopathy, is well recognized and has been reviewed elsewhere. However, TNFα also has profound effects on vascular smooth muscle cells (VSMCs) including a fundamental change from a contractile to a secretory phenotype. This "phenotypic switching" promotes proliferation and production of extracellular matrix proteins which are associated with medial hypertrophy. Additionally, it promotes lipid storage and enhanced motility, changes that support the contribution of VSMCs to neointima and atherosclerotic plaque formation. This review focuses on the role of TNFα in driving the inflammatory changes in VSMC biology that contribute to cardiovascular disease. Special attention is given to the mechanisms by which TNFα promotes ROS production at specific subcellular locations, and the contribution of these ROS to TNFα signaling.
    MeSH term(s) Animals ; Atherosclerosis/metabolism ; Humans ; Hypertension/metabolism ; Muscle, Smooth, Vascular/cytology ; Myocytes, Smooth Muscle/metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction ; Tumor Necrosis Factor-alpha/metabolism
    Chemical Substances Reactive Oxygen Species ; Tumor Necrosis Factor-alpha
    Language English
    Publishing date 2020-06-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 639383-4
    ISSN 1941-7225 ; 1879-1905 ; 0895-7061
    ISSN (online) 1941-7225 ; 1879-1905
    ISSN 0895-7061
    DOI 10.1093/ajh/hpaa089
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    Zs.A 2329: Show issues Location:
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  10. Article ; Online: Modulation of ClC-3 gating and proton/anion exchange by internal and external protons and the anion selectivity filter.

    Rohrbough, Jeffrey / Nguyen, Hong-Ngan / Lamb, Fred S

    The Journal of physiology

    2018  Volume 596, Issue 17, Page(s) 4091–4119

    Abstract: Key points: The ClC-3 2Cl: Abstract: We utilized plasma membrane-localized ClC-3 to investigate relationships between steady-state transport current ( ... ...

    Abstract Key points: The ClC-3 2Cl
    Abstract: We utilized plasma membrane-localized ClC-3 to investigate relationships between steady-state transport current (I
    MeSH term(s) Anions/metabolism ; Cell Membrane/metabolism ; Chloride Channels/genetics ; Chloride Channels/metabolism ; Glutamic Acid/metabolism ; HEK293 Cells ; Humans ; Hydrogen-Ion Concentration ; Ion Channel Gating ; Ion Transport ; Kinetics ; Mutation ; Protons ; Tyrosine/genetics ; Tyrosine/metabolism
    Chemical Substances Anions ; CLC-5 chloride channel ; Chloride Channels ; ClC-3 channel ; Protons ; Glutamic Acid (3KX376GY7L) ; Tyrosine (42HK56048U)
    Language English
    Publishing date 2018-07-29
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 3115-x
    ISSN 1469-7793 ; 0022-3751
    ISSN (online) 1469-7793
    ISSN 0022-3751
    DOI 10.1113/JP276332
    Database MEDical Literature Analysis and Retrieval System OnLINE

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