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  • Ovid Technologies (Wolters Kluwer Health)  (17)
  • 2010-2014  (17)
  • 1
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    Abstract 001: Axl Expression by CD4+ T Lymphocytes Promotes Salt-Dependent Hypertension
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Hypertension Vol. 64, No. suppl_1 ( 2014-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 64, No. suppl_1 ( 2014-09)
    Abstract: Introduction: Our laboratory has shown that Axl, a receptor tyrosine kinase, is important in both vascular and immune functions during deoxycorticosterone acetate (DOCA)-salt hypertension. We hypothesized that Axl activity specifically in T lymphocytes could explain the dependence of hypertension on Axl. Methods and Results: We did adoptive transfers of either Axl+/+ or Axl-/- CD4+ T cells to RAG1-/- mice that lack mature T cells. Once CD4+ T cell repopulations were confirmed, we induced DOCA-salt hypertension for 6 weeks. Systolic blood pressure (BP, mmHg) increased by 20±5 in Axl+/+RAG-/- mice after DOCA-salt, but Axl-/- RAG-/- mice had increases in BP by only 6+3 after 6 weeks of DOCA-salt. We isolated naïve CD4+ T cells from both Axl+/+ and Axl-/- littermates and primed them under either Th1 or Th2 polarizing conditions in culture. Production of interferon gamma (IFN-γ ng/mL) was significantly decreased (-23%, p 〈 0.05) in Axl-/- (396±23) compared to Axl+/+ (512±42) under Th1-priming. However, Axl had no effect on interleukin 4 (IL-4, ng/mL) production under Th2 polarizing conditions. Intracellular staining of the Th1/Th2 cells with IFN-γ and IL-4 antibodies by flow cytometry confirmed expression of cytokines in culture media. Complete blood counts showed that Axl-/- mice had significantly lower white blood cells due to decreased numbers of lymphocytes (4.5±0.7x10 9 ) compared to Axl+/+ mice (7.8±0.7x10 9 ). We found a higher population of AnnexinV (marker of early apoptosis)-positive peripheral leukocytes in Axl-/- mice (10±1%) compared to Axl+/+ (4±1%) by flow cytometry; while the percentages of dead cells (~10%) were similar between Axl+/+ and Axl-/- mice. Conclusions: Altogether we show that expression of Axl by T cells drives salt-induced hypertension. The mechanism of Axl-dependent effects on T cells occurs via T-cell-dependent expression of the pro-inflammatory cytokine IFN-γ. In addition, Axl plays a role in inhibiting lymphocyte apoptosis in the circulation. Future work will focus on how Axl expression in T cells affects T cell-dependent vascular remodeling during hypertension.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.64.suppl_1.001
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 2094210-2
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  • 2
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    Abstract 359: Hemodynamic Differences in Normal and Stress Conditions between SJL/J and C3HeB/FeJ Inbred Mouse Strains
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Hypertension Vol. 60, No. suppl_1 ( 2012-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 60, No. suppl_1 ( 2012-09)
    Abstract: Introduction: SJL/J (SJL) mice have elevated (80beats/min) heart rate (HR) compared to C3HeB/FeJ (C3HeB) mouse strain then measured by tail-cuff plethysmography. SJL and C3HeB are differed in behavioral phenotypes. The goal of this study was to investigate hemodynamic responses to normal and stress conditions between SJL and C3HeB inbred mouse strains. Methods and Results: Radio telemetry was used for continuous recordings of HR and systolic blood pressure (SBP) in C3HeB (n=5-10) and SJL (n=4-10) mice. We found that both strains showed normal circadian rhythms with little differences in HR and SBP. However, a locomotor activity (LA) of SJL was lower compared to C3HeB (7.8±0.4 vs. 10.0±0.1counts) during the lights off period. A correlation between LA and HR was reduced in SJL (R 2 =0.27) compared to C3HeB (R 2 =0.67) during the lights off period. After a mild stress (transfer to a cage) SJL had a slight HR elevation (70 beats/min) compared to C3HeB in first 5min. LA and SBP were similar between inbred strains after a novel cage test. The HR changes were significantly higher (2.5-fold, p 〈 0.05) in SJL vs. C3HeB during first 5min (30min of restraining period) on the first day of tail-cuff training. Five days of tail-cuff procedures resulted in 2-fold elevation of HR in SJL compared to C3HeB for 30min restraining period. Interestingly, changes in SBP were similar between mouse strains on first day, while SBP showed a trend to be 2-fold higher in SJL vs. C3HeB for 30min on day five. Autonomic control of HR was determined by pharmacological blockages in mice. Atropine (1mg/kg, i.p.) caused significantly greater increases in HR in SJL (160+8beats/min, p 〈 0.05) compared to C3HeB (62+11beats/min). Administration of propranolol (4mg/kg, i.p.) resulted in similar HR reductions between these strains. Conclusions: We found that SJL mice are susceptible to elevation of hemodynamic parameters after chronic stress. An increase in sympathetic nervous system activity may explain HR differences between SJL and C3HeB inbred strains. This study was supported in part by funds from Russian Program "Scientific and scientific-pedagogical personnel of innovative Russia" for 2009-2013 GK№14.740.11.0923 and HL105623 (VAK)
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.60.suppl_1.A359
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 2094210-2
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  • 3
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    Abstract 317: A Congenic Mouse Model for Carotid Intima-Media Thickening Demonstrates that Leukocyte Infiltration is a Genetically Regulated Trait
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 33, No. suppl_1 ( 2013-05)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 33, No. suppl_1 ( 2013-05)
    Abstract: We demonstrated that inflammation and intima-media thickening (IMT) are increased in carotids exposed to low blood flow in the SJL/J (SJL) mouse strain compared to other strains. We identified three novel quantitative trait loci (QTLs) on chromosomes (chr) 2, 11, and 18 that control IMT in a genetic cross between C3HeB/FeJ (C3H/F) and SJL mice. Using a genetic backcross of C3H/FxSJL we measured inflammation in carotid IMT as a quantitative trait. Immunostaining for CD45+ (a pan-specific leukocyte marker) was performed on carotids from C3H/F, SJL, F1 and N2 progeny to measure leukocyte infiltration. A QTL for CD45+ cell infiltration was identified on chr11 (17cM, LOD=2.3). Interval mapping showed that the CD45+ locus accounted for 8% of the variation in the C3H/FxSJL backcross. Importantly, the CD45+ locus co-localized with our previously reported intima modifier 2 (Im2) locus. We created two Im2 congenic mice (C3H/F.SJL.11.1 and C3H/F.SJL.11.2) to define the contribution of chr11 to IMT. The C3H/F.SJL.11.1 congenic mouse showed elevated CD45+ staining in the vascular wall in response to low flow. Thus, the CD45+ trait partially explains the intima trait. This reveals a potential mechanistic relationship between leukocyte infiltration and IMT in response to decreased blood flow.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.33.suppl_1.A317
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
    detail.hit.zdb_id: 1494427-3
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  • 4
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    Molecular approaches to ependymoma : the next step(s)
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Current Opinion in Neurology Vol. 25, No. 6 ( 2012-12), p. 745-750
    Details
    In: Current Opinion in Neurology, Ovid Technologies (Wolters Kluwer Health), Vol. 25, No. 6 ( 2012-12), p. 745-750
    Type of Medium: Online Resource
    ISSN: 1350-7540
    URL: Article
    DOI: 10.1097/WCO.0b013e328359cdf5
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 2026967-5
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  • 5
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    Sorafenib Plus Valproic Acid for Infant Spinal Glioblastoma
    Ovid Technologies (Wolters Kluwer Health) ; 2010
    In:  Journal of Pediatric Hematology/Oncology Vol. 32, No. 6 ( 2010-08), p. 511-514
    Details
    In: Journal of Pediatric Hematology/Oncology, Ovid Technologies (Wolters Kluwer Health), Vol. 32, No. 6 ( 2010-08), p. 511-514
    Type of Medium: Online Resource
    ISSN: 1077-4114
    URL: Article
    DOI: 10.1097/MPH.0b013e3181d74702
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2010
    detail.hit.zdb_id: 2047125-7
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  • 6
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    Novel tyrosine kinase signaling pathways : implications in vascular remodeling
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Current Opinion in Nephrology and Hypertension Vol. 21, No. 2 ( 2012-03), p. 122-127
    Details
    In: Current Opinion in Nephrology and Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 21, No. 2 ( 2012-03), p. 122-127
    Type of Medium: Online Resource
    ISSN: 1062-4821
    URL: Article
    DOI: 10.1097/MNH.0b013e3283503ce9
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 2029133-4
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  • 7
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    Abstract 566: A Genetic Locus on Mouse Chromosome 11 controls Endothelial Dysfunction
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Hypertension Vol. 64, No. suppl_1 ( 2014-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 64, No. suppl_1 ( 2014-09)
    Abstract: Introduction: Carotid intima formation is a significant risk factor for cardiovascular disease. C3H/FeJ (C3H/F) and SJL/J (SJL) inbred mouse strains differ in susceptibility to immune and vascular traits. Using a congenic approach we demonstrated that the Intima modifier 2 ( Im 2) locus on chromosome 11 regulates leukocyte infiltration. We sought to determine whether inflammation was due to changes in circulating immune cells or activation of vascular wall cells in genetically pure Im 2 (C3H/F.SJL.11.1) mice. Methods and Results: Complete blood counts showed no differences in circulating cells between C3H/F and C3H/F.SJL.11.1 compared to SJL mice. Aortic vascular cell adhesion molecule-1 (VCAM-1) total protein levels were dramatically increased in SJL and C3H/F.SJL.11.1 compared to C3H/F mice. Immunostaining of aortic endothelial cells (EC) showed a significant increase in VCAM-1 expression area (um 2 ) in SJL (0.18±0.02) and C3H/F.SJL.11.1 (0.19±0.02) compared to C3H/F (0.09±0.02) under steady flow conditions. In regions of disturbed flow we observed a significant decrease in EC area, measured by membrane staining, in SJL (500±50) and C3H/F.SJL.11.1 (500±30) versus C3H/F (800±50). Vascular permeability measured by the Miles assay (Evans’ blue dye ug per mg of aorta) was significantly higher in SJL (0.043±0.006) compared to C3H/F (0.010±0.005). In C3H/F.SJL.11.1 congenic mice vascular permeability varied from 0.006 to 0.665 but the average trended toward SJL values. Conclusions: Our results indicate that Im 2 regulation of leukocyte infiltration is mediated by EC inflammation and permeability. Comparative analysis of gene polymorphisms in human regions syntenic with the mouse Im 2 locus provides new insights into candidate genes that regulate vascular wall inflammation.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.64.suppl_1.566
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 2094210-2
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  • 8
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    Gas6-Axl Pathway : The Role of Redox-Dependent Association of Axl With Nonmuscle Myosin IIB
    Ovid Technologies (Wolters Kluwer Health) ; 2010
    In:  Hypertension Vol. 56, No. 1 ( 2010-07), p. 105-111
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 56, No. 1 ( 2010-07), p. 105-111
    Abstract: In vascular smooth muscle cells, Axl is a key receptor tyrosine kinase, because it is upregulated in injury, increases migration and neointima formation, and is activated by reactive oxygen species. Reaction of glutathione with cysteine residues (termed “glutathiolation”) is an important posttranslational redox modification that may alter protein activity and protein-protein interactions. To investigate the mechanisms by which reactive oxygen species increase Axl-dependent vascular smooth muscle cell function we assayed for glutathiolated proteins that associated with Axl in a redox-dependent manner. We identified glutathiolated nonmuscle myosin heavy chain (MHC)-IIB as a novel Axl interacting protein. This interaction was specific in that other myosins did not interact with Axl. The endogenous ligand for Axl, Gas6, increased production of reactive oxygen species in vascular smooth muscle cells and also increased the association of Axl with MHC-IIB. Antioxidants ebselen and N-acetylcysteine decreased the association of Axl with MHC-IIB in response to both Gas6 and reactive oxygen species. Blocking the Axl–MHC-IIB interaction with the specific myosin II inhibitor blebbistatin decreased phosphorylation of Axl and activation of extracellular signal–regulated kinase 1/2 and Akt. Association of MHC-IIB with Axl was increased in balloon-injured rat carotid vessels. Finally, expression of MHC-IIB was upregulated in the neointima of the carotid artery after balloon injury similar to upregulation of Axl protein expression, as shown in our previous studies. These results demonstrate a novel interaction between Axl and MHC-IIB in response to reactive oxygen species. This interaction provides a direct link between Axl and molecular motors crucial for directed cell migration, which may mediate increased migration in vascular dysfunction.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.109.144642
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2010
    detail.hit.zdb_id: 2094210-2
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  • 9
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    Ribosomal Protein L17, RpL17, is an Inhibitor of Vascular Smooth Muscle Growth and Carotid Intima Formation
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Circulation Vol. 126, No. 20 ( 2012-11-13), p. 2418-2427
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 126, No. 20 ( 2012-11-13), p. 2418-2427
    Abstract: Carotid intima-media thickening is associated with increased cardiovascular risk in humans. We discovered that intima formation and cell proliferation in response to carotid injury is greater in SJL/J (SJL) in comparison with C3HeB/FeJ (C3H/F) mice. The purpose of this study was to identify candidate genes contributing to intima formation. Methods and Results— We performed microarray and bioinformatic analyses of carotid arteries from C3H/F and SJL mice. Kyoto Encyclopedia of Genes and Genomes analysis showed that the ribosome pathway was significantly up-regulated in C3H/F in comparison with SJL mice. Expression of a ribosomal protein, RpL17, was 〉 40-fold higher in C3H/F carotids in comparison with SJL. Aortic vascular smooth muscle cells from C3H/F grew slower in comparison to SJL. To determine the role of RpL17 in vascular smooth muscle cell growth regulation, we analyzed the relationship between RpL17 expression and cell cycle progression. Cultured vascular smooth muscle cells from mice, rats, and humans showed that RpL17 expression inversely correlated with growth as shown by decreased cells in S phase and increased cells in G 0 /G 1 . To prove that RpL17 acted as a growth inhibitor in vivo, we used pluronic gel delivery of RpL17 small interfering RNA to C3H/F carotid arteries. This resulted in an 8-fold increase in the number of proliferating cells. Furthermore, following partial carotid ligation in SJL mice, RpL17 expression in the intima and media decreased, but the number of proliferating cells increased. Conclusions— RpL17 acts as a vascular smooth muscle cell growth inhibitor (akin to a tumor suppressor) and represents a potential therapeutic target to limit carotid intima-media thickening.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.112.125971
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 1466401-X
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  • 10
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    Role of Axl in Early Kidney Inflammation and Progression of Salt-Dependent Hypertension
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Hypertension Vol. 62, No. 2 ( 2013-08), p. 302-309
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 62, No. 2 ( 2013-08), p. 302-309
    Abstract: The Gas6/Axl pathway regulates many cell functions and is implicated in hypertension. In this study, we aimed to investigate the role of Axl in immune cells on initiation and progression of salt-dependent hypertension. Deoxycorticosterone acetate (75 mg/60 days release)–salt hypertension was induced for 1 week or 6 weeks in Axl chimeras generated by bone marrow transplant to restrict Axl deficiency to hematopoietic or nonhematopoietic compartments. Depletion of Axl in hematopoietic cells (Axl −/− →Axl +/+ ) reduced (133±2 mm Hg) increase in systolic blood pressure compared with other Axl chimeras (≈150 mm Hg) 1 week after deoxycorticosterone acetate–salt. Urine protein and renal oxidative stress were lowest in Axl −/− →Axl +/+ at 1 week after deoxycorticosterone acetate–salt. Compensatory increase in Gas6 in kidneys of recipient Axl −/− may affect kidney function and blood pressure in early phase of hypertension. Flow cytometry on kidneys from Axl −/− →Axl +/+ showed increase in total leukocytes, B, and dendritic cells and decrease in macrophages compared with Axl +/+ →Axl +/+ . These immune changes were associated with decrease in proinflammatory gene expression, in particular interferon γ. Systolic blood pressure returned to baseline in Axl −/− →Axl +/+ and Axl −/− →Axl −/− but remained increased in Axl +/+ →Axl +/+ and Axl +/+ →Axl −/− chimeras after 6 weeks of deoxycorticosterone acetate–salt. Vascular apoptosis was increased in the global Axl −/− chimeras in the late phase of hypertension. In summary, we found that expression of Axl in hematopoietic cells is critical for kidney pathology in early phase of salt-dependent hypertension. However, Axl in both hematopoietic and nonhematopoietic lineages contributes to the late phase of hypertension.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.113.01382
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
    detail.hit.zdb_id: 2094210-2
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