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  • 1
    Online Resource
    Online Resource
    Increased risk of severe COVID-19 in hospitalized patients with SARS-CoV-2 Alpha variant infection: a multicentre matched cohort study
    Springer Science and Business Media LLC ; 2022
    In:  BMC Infectious Diseases Vol. 22, No. 1 ( 2022-12)
    Details
    In: BMC Infectious Diseases, Springer Science and Business Media LLC, Vol. 22, No. 1 ( 2022-12)
    Abstract: The impact of the variant of concern (VOC) Alpha on the severity of COVID-19 has been debated. We report our analysis in France. Methods We conducted an exposed/unexposed cohort study with retrospective data collection, comparing patients infected by VOC Alpha to contemporaneous patients infected by historical lineages. Participants were matched on age (± 2.5 years), sex and region of hospitalization. The primary endpoint was the proportion of hospitalized participants with severe COVID-19, defined as a WHO-scale  〉  5 or by the need of a non-rebreather mask, occurring up to day 29 after admission. We used a logistic regression model stratified on each matched pair and accounting for factors known to be associated with the severity of the disease. Results We included 650 pairs of patients hospitalized between Jan 1, 2021, and Feb 28, 2021, in 47 hospitals. Median age was 70 years and 61.3% of participants were male. The proportion of participants with comorbidities was high in both groups (85.0% vs 90%, p = 0.004). Infection by VOC Alpha was associated with a higher odds of severe COVID-19 (41.7% vs 38.5%—aOR = 1.33 95% CI [1.03–1.72]). Conclusion Infection by the VOC Alpha was associated with a higher odds of severe COVID-19.
    Type of Medium: Online Resource
    ISSN: 1471-2334
    URL: Article
    DOI: 10.1186/s12879-022-07508-x
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2041550-3
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  • 2
    Online Resource
    Online Resource
    High Pressure Promotes Monocyte Adhesion to the Vascular Wall
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Circulation Research Vol. 100, No. 8 ( 2007-04-27), p. 1226-1233
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 100, No. 8 ( 2007-04-27), p. 1226-1233
    Abstract: Hypertension is a known risk factor for the development of atherosclerosis. To assess how mechanical factors contribute to this process, mouse carotid arteries were maintained in organ culture at normal (80 mm Hg) or high (150 mm Hg) intraluminal pressure for 1, 6, 12, or 24 hours. Thereafter, fluorescent human monocytic cells (U937) were injected intraluminally and allowed to adhere for 30 minutes before washout. U937 adhesion was increased in vessels kept at 150 mm Hg 12 hours (23.5±5.7 versus 9.9±2.2 cells/mm at 80 mm Hg; P 〈 0.05) or 24 hours (26.7±5.7 versus 8.8±1.5 cells/mm; P 〈 0.05). At 24 hours, high pressure was associated with increased mRNA expression of monocyte chemoattractant protein-1, interleukin-6, keratinocyte-derived chemokine, and vascular cell adhesion molecule-1 (6.9±2.1, 4.4±0.1, 9.8±2.8, and 2.4±0.1-fold respectively; P 〈 0.05), as assessed by quantitative RT-PCR and corroborated by immunohistochemistry, which also revealed an increase in intracellular adhesion molecule-1 expression. Nuclear factor κB inhibition using SN50 peptide abolished the overexpression of chemokines and adhesion molecules and reduced U937 adhesion in vessels at 150 mm Hg. Moreover, treatment of vessels and cells with specific neutralizing antibodies established that monocyte chemoattractant protein-1, interleukin-6, and keratinocyte-derived chemokine released from vessels at 150 mm Hg primed the monocytes, increasing their adhesion to vascular cell adhesion molecule-1 but not intracellular adhesion molecule-1 via α 4 β 1 integrins. The additive effect of chemokines on the adhesion of U937 cells to vascular cell adhesion molecule-1 was confirmed by in vitro assay. Finally, pressure-dependent U937 adhesion was blunted in arteries from mice overexpressing endothelial NO synthase. Hence, high intraluminal pressure induces cytokine and adhesion molecule expression via nuclear factor κB, leading to monocytic cell adhesion. These results indicate that hypertension may directly contribute to the development of atherosclerosis through nuclear factor κB induction.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.0000265231.59354.2c
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
    detail.hit.zdb_id: 1467838-X
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  • 3
    Online Resource
    Online Resource
    Abstract 876: Combined Inhibition Of Ccl2, Cx3cr1 And Ccr5 Abrogates Ly6chi And Ly6clo Monocytosis And Almost Abolishes Atherosclerosis In Hypercholesterolemic Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Circulation Vol. 116, No. suppl_16 ( 2007-10-16)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 116, No. suppl_16 ( 2007-10-16)
    Abstract: Monocytes are critical mediators of atherogenesis. Specialized chemokine/chemokine receptor pathways orchestrate the infiltration of specific monocyte subsets within atherosclerotic arteries. Interruption of individual chemokine pathways including CCL2/CCR2, CCL5/CCR5, CX3CL1/CX3CR1, CXCL8/CXCR2 or CXCL10/CXCR3, leads to significant but only partial inhibition of lesion development, whereas deficiency in other signals such as CXCL16 or CCR1 accelerates atherosclerosis. Evidence that particular chemokine pathways may cooperate to promote monocyte recruitment into atherosclerotic arteries is still lacking. Here, we show that in addition to the current prevailing paradigm accounting for the role of chemokines as modulators of monocyte trafficking between the blood and the vessel wall, chemokine-mediated signals critically determine the frequency of monocytes in the blood and the bone marrow under both non-inflammatory and atherosclerotic conditions. Particularly, CCL2, CX3CR1 and CCR5-dependent signals differentially alter CD11b+ Ly6G- 7/4hi (also known as Ly6Chi) and CD11b + Ly6G- 7/4lo (Ly6Clo) monocytosis. Combined inhibition of these pathways in hypercholesterolemic, atherosclerosis susceptible apolipoprotein E-deficient mice leads to additive reduction in bone marrow and circulating monocytes, associated with a marked and additive 90% reduction in atherosclerosis. Lesion size highly correlates with the number of circulating monocytes. Thus, signals mediated through CCL2, CX3CR1 and CCR5 critically determine the frequency of circulating monocyte subsets and thereby account for almost all macrophage accumulation into atherosclerotic arteries.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.116.suppl_16.II_171-b
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
    detail.hit.zdb_id: 1466401-X
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  • 4
    Online Resource
    Online Resource
    Role of NF-κB in Flow-Induced Vascular Remodeling
    Mary Ann Liebert Inc ; 2009
    In:  Antioxidants & Redox Signaling Vol. 11, No. 7 ( 2009-07), p. 1641-1649
    Details
    In: Antioxidants & Redox Signaling, Mary Ann Liebert Inc, Vol. 11, No. 7 ( 2009-07), p. 1641-1649
    Type of Medium: Online Resource
    ISSN: 1523-0864 , 1557-7716
    URL: Article
    DOI: 10.1089/ars.2008.2393
    Language: English
    Publisher: Mary Ann Liebert Inc
    Publication Date: 2009
    detail.hit.zdb_id: 2039747-1
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  • 5
    Online Resource
    Online Resource
    Gas6 Promotes Pro-Inflammatory (Ly6Chi) Monocyte Recruitment in Venous Thrombosis
    American Society of Hematology ; 2014
    In:  Blood Vol. 124, No. 21 ( 2014-12-06), p. 1533-1533
    Details
    In: Blood, American Society of Hematology, Vol. 124, No. 21 ( 2014-12-06), p. 1533-1533
    Abstract: Recent studies have demonstrated that innate immune cells, i.e. neutrophils and monocytes, provide the initiating stimulus for venous thrombus development. Gas6 was found to promote inflammation by inducing interactions between the endothelium and innate immune cells. In addition, we recently showed that Gas6 was involved in venous thrombosis by inducing tissue factor expression in the endothelium. Since Gas6 is expressed in monocytes, we hypothesize that Gas6 may be involved in monocyte recruitment during venous thrombosis. Venous thrombosis was induced in the inferior vena cava of wild type (WT) and Gas6 deficient (-/-) mice using 5% FeCl3. Using ultrasonography, we found that global monocyte depletion by clodronate resulted in the formation of smaller thrombi. Selective depletion of the pro-inflammatory (Ly6Chi) monocyte subset, using an anti-CCR2 antibody, also induced the formation of smaller clots. In addition, MOMA-2 (monocyte-macrophage marker) staining showed a reduced number of monocytes in thrombi from Gas6-/- mice. More importantly, immunofluorescent staining revealed that fewer Ly6Chi monocytes were recruited to the thrombi of Gas6-/- mice compared to WT. However, Ly6Clow (patrolling) monocytes were equivalently recruited between Gas6-/- and WT mice. In vitro, mRNA expression of CCR2 was increased by thrombin in WT but not in Gas6-/- monocytes. The mRNA and protein expression of the CCR2 ligand, CCL2, was also increased by thrombin in WT but not in Gas6-/- endothelial cells. CCL2 secretion, as demonstrate by ELISA, was induced by thrombin treatment in WT but not in Gas6-/- endothelial cells. Conditioned media from WT or Gas6-/- endothelial treated by thrombin was used for monocyte migration experiments. The conditioned media from WT endothelial cells treated with thrombin increased migration of WT monocytes compared to media from untreated or Gas6-/- endothelial cells. Our results demonstrate an important role for Ly6Chi monocytes in thrombus formation and that Gas6 is specifically involved in the recruitment of these monocytes through the expression of CCL2 and CCR2. Disclosures No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V124.21.1533.1533
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2014
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 6
    Online Resource
    Online Resource
    Abstract 12315: Four-and-a-Half LIM Domain Protein-2 Absence Reduces Atherogenesis in Apolipoprotein E-deficient Mice: Role of Monocytic Immune Cells
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation Vol. 130, No. suppl_2 ( 2014-11-25)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 130, No. suppl_2 ( 2014-11-25)
    Abstract: Background: Four-and-a-half LIM domain protein-2 (FHL2) is expressed in endothelial and vascular smooth muscle cells. It negatively regulates endothelial cell survival and migration, but its role in atherogenesis is unknown. Methods and Results: FHL2-deficient (FHL2-/-) mice were crossed with apolipoprotein E-deficient (ApoE-/-) mice to generate ApoE/FHL2-/- mice. After high-fat, high-cholesterol diet, ApoE/FHL2-/- mice displayed significantly smaller atherosclerotic plaques than ApoE-/- mice in the aortic sinus, the brachiocephalic artery and the aorta. This was associated with significantly enhanced collagen and smooth muscle cell contents and a significant 2-fold reduction of macrophage content within the plaques of ApoE/FHL-2-/- vs ApoE-/- mice. There was a significant reduction in aortic ICAM-1 mRNA and VCAM-1 protein expression in the plaques of ApoE/FHL2-/- mice. Aortic gene expression of CX3CL1 and CCL5 was significantly increased in ApoE/FHL2-/- vs ApoE-/- mice. Peritoneal thioglycollate injection elicited equivalent numbers of monocytes and macrophages in both groups, but a significantly lower number of pro-inflammatory Ly6C-high monocytes were recruited in ApoE/FHL2-/- vs ApoE-/- mice. Furthermore, mRNA levels of CX3CR1 were 2-fold higher in monocytes from ApoE/FHL2-/- vs ApoE-/- mice. Finally, we investigated the potential importance of myeloid cell FHL2 deficiency in atherosclerosis. After being irradiated, ApoE-/- or ApoE/FHL2-/- mice were transplanted with ApoE-/- or ApoE/FHL2-/- bone marrow. After high-fat, high-cholesterol diet, both chimeric groups developed significantly smaller plaques than ApoE-/- mice transplanted with ApoE-/- bone marrow. Conclusion: These results suggest that FHL2 in both myeloid and vascular cells may play an important role in atherogenesis by promoting pro-inflammatory chemokine production, adhesion molecule expression, and pro-inflammatory monocyte recruitment.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.130.suppl_2.12315
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 1466401-X
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  • 7
    Online Resource
    Online Resource
    Chronic Physiological Shear Stress Inhibits Tumor Necrosis Factor–Induced Proinflammatory Responses in Rabbit Aorta Perfused Ex Vivo
    Ovid Technologies (Wolters Kluwer Health) ; 2003
    In:  Circulation Vol. 108, No. 13 ( 2003-09-30), p. 1619-1625
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 108, No. 13 ( 2003-09-30), p. 1619-1625
    Abstract: Background— Regions in the vasculature exposed to steady laminar flow have a lower likelihood for atherosclerosis than regions exposed to disturbed flow with low shear stress. We previously found that laminar flow of short duration inhibited tumor necrosis factor (TNF)-α–mediated proinflammatory signaling in cultured endothelial cells (ECs). However, mechanisms responsible for the atheroprotective effects of physiological shear stress remain undefined. Therefore, we examined the effects of chronic shear stress on TNF-α–induced inflammatory responses using an ex vivo perfusion organ culture system. Methods and Results— Rabbit aortas were exposed to low or normal shear stress (0.4 or 12 dyne/cm 2 ) at a constant pressure for 24 to 26 hours. EC and vascular smooth muscle cell (VSMC) proteins were selectively purified. After exposure to low shear stress, TNF-α (50 ng/mL, 6 hours) specifically stimulated vascular cell adhesion molecule (VCAM)-1 expression in ECs but not VSMCs. TNF-α–stimulated VCAM expression was inhibited significantly by preexposure to normal shear stress. Normal shear stress inhibited TNF (15 minutes) activation of mitogen-activated protein (MAP) kinases (c-Jun NH 2 -terminal kinase [JNK], p38, extracellular signal–regulated kinase [ERK] ) in ECs. Specific pharmacological inhibitors of JNK and p38 but not ERK significantly inhibited TNF-induced VCAM expression. Normal shear stress prevented the association of TNF receptor (TNFR)-1 with TNFR-associated factor (TRAF)-2. There was no effect of low or normal shear stress on TNF-α–induced nuclear factor-κB activation. A nitric oxide synthesis inhibitor, N G -nitro- l -arginine methyl ester, did not reverse the inhibitory effects of shear stress on VCAM expression. Conclusions— These results suggest that physiological shear stress is antiinflammatory by specifically inhibiting MAP kinase signaling and inhibiting TRAF-2 interaction with TNFR-1.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.0000089373.49941.C4
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2003
    detail.hit.zdb_id: 1466401-X
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  • 8
    Online Resource
    Online Resource
    Adventures in the Adventitia
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Hypertension Vol. 67, No. 5 ( 2016-05), p. 836-838
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 67, No. 5 ( 2016-05), p. 836-838
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.116.06375
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 2094210-2
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  • 9
    Online Resource
    Online Resource
    Inhibition of Four-and-a-Half LIM Domain Protein-2 Increases Survival, Migratory Capacity, and Paracrine Function of Human Early Outgrowth Cells Through Activation of the Sphingosine Kinase-1 Pathway : Implications for Endothelial Regeneration
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation Research Vol. 114, No. 1 ( 2014-01-03), p. 114-123
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 114, No. 1 ( 2014-01-03), p. 114-123
    Abstract: Inhibition of four-and-a-half LIM domain protein-2 (FHL2) attenuates atherosclerotic lesion formation and increases endothelial cell migration. Early outgrowth cells (EOCs) contribute substantially to endothelial repair. Objective: We investigated the role of FHL2 in the regulation of EOCs. Methods and Results: Human EOCs were cultured from peripheral blood. FHL2 knockdown in EOCs by siRNA resulted in increased EOC numbers and reduced apoptosis, as indicated by decreased cleaved caspase-III and reduced Bax/Bcl-2 expression ratio. This was mediated through increased phosphorylation and membrane translocation of sphingosine kinase-1, increased sphingosine-1-phosphate levels, and Akt phosphorylation. FHL2 knockdown increased stromal cell–derived factor-1–induced EOC migration through upregulation of αv/β3, αv/β5, and β2 integrins, associated with increased cortactin expression. Reduced apoptosis, increased EOC migration, and cortactin upregulation by FHL2 siRNA were prevented by CAY10621, the sphingosine kinase-1 inhibitor, and the sphingosine-1-phosphate receptor-1/-3 antagonist VPC23019. These findings were confirmed using spleen-derived EOCs from FHL2 −/− mice. Apoptosis was decreased and migration increased in endothelial cells exposed to the conditioned medium of FHL2 −/− versus wild-type (WT) EOCs. These paracrine effects were abolished by VPC23019. Importantly, reendothelialization after focal carotid endothelial injury in WT mice was significantly increased after intravenous injection of FHL2 −/− versus WT EOCs. Conclusions: Our findings suggest that FHL2 negatively regulates EOC survival, migration, and paracrine function. FHL2 inhibition in EOCs reduces apoptosis and enhances survival and migratory capacity of both EOCs and surrounding endothelial cells by activation of the sphingosine kinase-1/sphingosine-1-phosphate pathway, resulting in improvement of endothelial regeneration.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.113.301954
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 1467838-X
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  • 10
    Online Resource
    Online Resource
    Signal Transduction of Mechanical Stresses in the Vascular Wall
    Ovid Technologies (Wolters Kluwer Health) ; 1998
    In:  Hypertension Vol. 32, No. 2 ( 1998-08), p. 338-345
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 32, No. 2 ( 1998-08), p. 338-345
    Abstract: Abstract —The vascular wall is constantly subjected to a variety of mechanical forces in the form of stretch (tensile stress), due to blood pressure, and shear stress, due to blood flow. Alterations in either of these stresses are known to result in vascular remodeling, an adaptation characterized by modified morphology and function of the blood vessels, allowing the vessels to cope with physiological or pathological conditions. The processes involved in vascular remodeling include cellular hypertrophy and hyperplasia, as well as enhanced protein synthesis or extracellular matrix protein reorganization. In vitro studies using vascular cells have attempted to identify the mechanisms behind structural alterations. Possible pathways include ion channels, integrin interaction between cells and the extracellular matrix, activation of various tyrosine kinases (such as c-Src, focal adhesion kinase, and mitogen-activated protein kinases), and autocrine production and release of growth factors. These pathways lie upstream of de novo synthesis of immediate response genes and total protein synthesis, both of which are likely to be involved in the process of vascular remodeling.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.32.2.338
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1998
    detail.hit.zdb_id: 2094210-2
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