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  • Ovid Technologies (Wolters Kluwer Health)  (15)
  • 1
    Online Resource
    Online Resource
    Abstract 712: Elastin Derived Peptides Augments Abdominal Aortic Aneurysm Formation
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 38, No. Suppl_1 ( 2018-05)
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 38, No. Suppl_1 ( 2018-05)
    Abstract: Abdominal aortic aneurysm AAA is a chronic dilatation of the abdominal aorta. It is a potentially life threatening disease as it develops asymptomatic and is often first discovered at the time of rupture. One key element in AAA formation is degradation of the elastin fibers in the aortic wall. When elastin is degraded small bioactive elastin derived peptides (EDPs) are released into the circulation. These EDPs affect vascular smooth muscle cells in the aortic wall and attract monocytes to the aortic wall resulting in further degradation of elastin. We hypothesize that the level of circulating elastin derived peptides (EDPs) augments AAA expansion and that inhibition of circulating EDPs will inhibit AAA expansion. We tested the hypothesis in an elastase induced aneurysm murine model by applying synthetic EDPs or scrambles peptides and measure the AAA size. In addition, EDP-neutralizing antibody or control IgG was given to angiotensin II induced AAA in ApoE-/- mice and AAA size was determined 28 days later. Fourteen days after elastase infusion the abdominal aortic diameter was significantly increased in the EDP treated group when compared to the scramble peptid treated control group (1.33±0.07 vs. 1.13±0.06 mm, n=17-19, p 〈 0.05). Inhibition of circulating EDPs by EDP neutralizing antibodies when compared to IgG controls showed a clear trend toward decreased AAA expansion based on outer aortic diameter (1.4 ±0.1 vs. 2.2 ±0.4 mm, n=8-9, p=0.059) and wet weights of the abdominal aorta (median: 9.2 vs. 22.1 mg, n=7-9, p=0.07) 28 days after angiotensin II infusion in ApoE-/- mice. In the aneurysmal wall of the mice treated with elastin neutralizing antibody, there was less ruptured elastin, and there was significantly fewer infiltrating of CD45 positive cells, while CD206 positive anti-inflammatory M2 macrophages were significantly augmented when compared to IgG treated controls (n=7-9).In conclusion, EDPs augment abdominal aortic aneurysms. Thus, inhibition of circulating EDPs shows great potential against AAA expansion.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.38.suppl_1.712
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 1494427-3
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  • 2
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    Induction of autoimmune abdominal aortic aneurysm in pigs - A novel large animal model
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Annals of Medicine & Surgery Vol. 20 ( 2017-08), p. 26-31
    Details
    In: Annals of Medicine & Surgery, Ovid Technologies (Wolters Kluwer Health), Vol. 20 ( 2017-08), p. 26-31
    Type of Medium: Online Resource
    ISSN: 2049-0801
    URL: Article
    DOI: 10.1016/j.amsu.2017.06.017
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 2745440-X
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  • 3
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    Cyclooxygenase-2–Dependent Prostacyclin Formation and Blood Pressure Homeostasis : Targeted Exchange of Cyclooxygenase Isoforms in Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2010
    In:  Circulation Research Vol. 106, No. 2 ( 2010-02-05), p. 337-345
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 106, No. 2 ( 2010-02-05), p. 337-345
    Abstract: Rationale : Cyclooxygenase (COX)-derived prostanoids (PGs) are involved in blood pressure homeostasis. Both traditional nonsteroidal antiinflammatory drugs (NSAIDs) that inhibit COX-1 and COX-2 and NSAIDs designed to be selective for inhibition of COX-2 cause sodium retention and elevate blood pressure. Objective : To elucidate the role of COX-2 in blood pressure homeostasis using COX-1 〉 COX-2 mice, in which the COX-1 expression is controlled by COX-2 regulatory elements. Methods and Results : COX-1 〉 COX-2 mice developed systolic hypertension relative to wild types (WTs) on a high-salt diet (HSD); this was attenuated by a PGI 2 receptor agonist. HSD increased expression of COX-2 in WT mice and of COX-1 in COX-1 〉 COX-2 mice in the inner renal medulla. The HSD augmented in all strains urinary prostanoid metabolite excretion, with the exception of the major PGI 2 metabolite that was suppressed on regular chow and unaltered by the HSD in both mutants. Furthermore, inner renal medullary expression of the receptor for PGI 2 , but not for other prostanoids, was depressed by HSD in WT and even more so in both mutant strains. Increasing osmolarity augmented expression of COX-2 in WT renal medullary interstitial cells and again the increase in formation of PGI 2 observed in WTs was suppressed in cells derived from both mutants. Intramedullary infusion of the PGI 2 receptor agonist increased urine volume and sodium excretion in mice. Conclusions : These studies suggest that dysregulated expression of the COX-2 dependent, PGI 2 biosynthesis/response pathway in the renal inner renal medulla undermines the homeostatic response to a HSD. Inhibition of this pathway may contribute directly to the hypertensive response to NSAIDs.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.109.204529
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2010
    detail.hit.zdb_id: 1467838-X
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  • 4
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    Ulcerating and stenosing enteropathy treated with misoprostol : a case report with analysis of prostaglandin metabolism
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  European Journal of Gastroenterology & Hepatology Vol. 24, No. 10 ( 2012-10), p. 1238-1241
    Details
    In: European Journal of Gastroenterology & Hepatology, Ovid Technologies (Wolters Kluwer Health), Vol. 24, No. 10 ( 2012-10), p. 1238-1241
    Type of Medium: Online Resource
    ISSN: 0954-691X
    URL: Article
    DOI: 10.1097/MEG.0b013e328356bc95
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 2030291-5
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  • 5
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    Plasmin in Nephrotic Urine Activates the Epithelial Sodium Channel
    Ovid Technologies (Wolters Kluwer Health) ; 2009
    In:  Journal of the American Society of Nephrology Vol. 20, No. 2 ( 2009-02), p. 299-310
    Details
    In: Journal of the American Society of Nephrology, Ovid Technologies (Wolters Kluwer Health), Vol. 20, No. 2 ( 2009-02), p. 299-310
    Type of Medium: Online Resource
    ISSN: 1046-6673
    URL: Article
    DOI: 10.1681/ASN.2008040364
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2009
    detail.hit.zdb_id: 2029124-3
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  • 6
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    Targeted Deletions of Cyclooxygenase-2 and Atherogenesis in Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2010
    In:  Circulation Vol. 121, No. 24 ( 2010-06-22), p. 2654-2660
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 121, No. 24 ( 2010-06-22), p. 2654-2660
    Abstract: Background— Although the dominant product of vascular Cyclooxygenase-2 (COX-2), prostacyclin (PGI 2 ), restrains atherogenesis, inhibition and deletion of COX-2 have yielded conflicting results in mouse models of atherosclerosis. Floxed mice were used to parse distinct cellular contributions of COX-2 in macrophages and T cells (TCs) to atherogenesis. Methods and Results— Deletion of macrophage–COX-2 (Mac–COX-2KOs) was attained with LysMCre mice and completely suppressed lipopolysaccharide-stimulated macrophage prostaglandin (PG) formation and lipopolysaccharide-evoked systemic PG biosynthesis by ≈30%. Lipopolysaccharide-stimulated COX-2 expression was suppressed in polymorphonuclear leukocytes isolated from MacKOs, but PG formation was not even detected in polymorphonuclear leukocyte supernatants from control mice. Atherogenesis was attenuated when MacKOs were crossed into hyperlipidemic low-density lipoprotein receptor knockouts. Deletion of Mac–COX-2 appeared to remove a restraint on COX-2 expression in lesional nonleukocyte (CD45- and CD11b-negative) vascular cells that express vascular cell adhesion molecule and variably α-smooth muscle actin and vimentin, portending a shift in PG profile and consequent atheroprotection. Basal expression of COX-2 was minimal in TCs, but use of CD4Cre to generate TC knockouts depressed its modest upregulation by anti-CD3ε. However, biosynthesis of PGs, TC composition in lymphatic organs, and atherogenesis in low-density lipoprotein receptor knockouts were unaltered in TC knockouts. Conclusions— Macrophage–COX-2, primarily a source of thromboxane A 2 and prostaglandin (PG)E 2 , promotes atherogenesis and exerts a restraint on enzyme expression by lesional cells suggestive of vascular smooth muscle cells, a prominent source of atheroprotective prostacyclin. TC COX-2 does not detectably influence TC development or function or atherogenesis in mice.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.109.910687
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2010
    detail.hit.zdb_id: 1466401-X
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  • 7
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    The mineralocorticoid receptor blocker spironolactone lowers plasma interferon-γ and interleukin-6 in patients with type 2 diabetes and treatment-resistant hypertension
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Journal of Hypertension Vol. 40, No. 1 ( 2022-01), p. 153-162
    Details
    In: Journal of Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 40, No. 1 ( 2022-01), p. 153-162
    Abstract: The mineralocorticoid receptor antagonist spironolactone lowers blood pressure in patients with resistant hypertension despite antihypertensive treatment with angiotensin-converting inhibitors (ACEi) and angiotensin-II receptor blockers (ARB). In preclinical studies, spironolactone suppresses pro-hypertensive interleukin 17A (IL-17A). Objectives: Plasma samples were analysed from a randomized, double-blind placebo-controlled trial with spironolactone given to patients with type 2 diabetes mellitus (T2DM) and resistant hypertension on three antihypertensive drugs. We tested the hypothesis that spironolactone-induced antihypertensive effects are associated with suppression of IL-17A and related cytokines. Methods: Interferon-γ (IFN-γ), IL-17A, tumor necrosis factor-α (TNF-α), IL-6, IL-1β and IL-10 were assessed in plasma with immunoassay in samples before and after 16 weeks of treatment with placebo or spironolactone (12.5-25–50 mg/day). Results: Spironolactone significantly reduced plasma IFN-γ and IL-6 while IL-17A, TNF-α, IL-1β and IL-10 were unchanged. IL-6 was more sensitive to higher doses of spironolactone. At baseline, serum aldosterone correlated positively with diastolic night blood pressure. Urine albumin/creatinine-ratios correlated positively with plasma IL-6 at baseline. There were no relations between aldosterone and cytokine concentrations at baseline; between cytokine concentration and blood pressure at baseline; and between cytokine concentration decrease and blood pressure decrease, except for IFN-γ, after treatment. The spironolactone-induced elevation in plasma potassium related inversely to blood pressure but not to changes in cytokines. In macrophages in vitro , spironolactone suppressed lipopolysaccharide (LPS)-induced TNF-α, IL-6, IL-1β and IL-10 levels. Conclusion: The antihypertensive action of spironolactone in resistant hypertensive patients is associated with suppressed IFN-γ and IL-6 and not IL-17A. Spironolactone exerts anti-inflammatory actions in vivo on macrophages and T-cells.
    Type of Medium: Online Resource
    ISSN: 0263-6352 , 1473-5598
    URL: Article
    DOI: 10.1097/HJH.0000000000002990
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 2017684-3
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  • 8
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    Prostaglandin I 2 and Prostaglandin E 2 Modulate Human Intrarenal Artery Contractility Through Prostaglandin E2-EP4, Prostacyclin-IP, and Thromboxane A2-TP Receptors
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Hypertension Vol. 64, No. 3 ( 2014-09), p. 551-556
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 64, No. 3 ( 2014-09), p. 551-556
    Abstract: Cyclooxygenase inhibitors decrease renal blood flow in settings with decreased effective circulating volume. The present study examined the hypothesis that prostaglandins, prostaglandin E 2 (PGE 2 ) and prostacyclin (PGI 2 ), induce relaxation of human intrarenal arteries through PGE 2 -EP and PGI 2 -IP receptors. Intrarenal arteries were microdissected from human nephrectomy samples (n=53, median diameter ≈362 μm, 88% viable, 76% relaxed in response to acetylcholine). Rings were suspended in myographs to record force development. In vessels with K + -induced tension (EC 70 : –log [mol/L]=1.36±0.03), PGE 2 and PGI 2 induced concentration-dependent relaxation (–log EC 50 : PGE 2 =7.1±0.3 and PGI 2 =7.7). The response to PGE 2 displayed endothelium dependence and desensitization. Relaxation by PGE 2 was mimicked by an EP4 receptor agonist (CAY10598, EC 50 =6.7±0.2). The relaxation after PGI 2 was abolished by an IP receptor antagonist (BR5064, 10 –8 mol/L). Pretreatment of quiescent arteries with PGE 2 for 5 minutes (10 –6 mol/L) led to a significant right shift of the concentration–response to norepinephrine (EC 50 from 6.6±0.1–5.9±0.1). In intrarenal arteries with K + -induced tone, PGE 2 and PGI 2 at 10 –5 mol/L elicited increased tension. This was abolished by thromboxane receptor (TP) antagonist (S18886, 10 –6 mol/L). A TP agonist (U46619, n=6) evoked tension (EC 50 =8.1±0.2) that was inhibited by S18886. Polymerase chain reaction and immunoblotting showed EP4, IP, and TP receptors in intrarenal arteries. In conclusion, PGE 2 and PGI 2 may protect renal perfusion by activating cognate IP and EP4 receptors associated with smooth muscle cells and endothelium in human intrarenal arteries and contribute to increased renal vascular resistance at high pathological concentrations mediated by noncognate TP receptor.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.113.03051
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 2094210-2
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  • 9
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    Abstract 598: Deletion of Microsomal PGE Synthase-1 Decreases Oxidative Stress and Protects Against Abdominal Aortic Aneurysm Formation in Angiotensin II-Infused 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: Microsomal (m) prostaglandin (PG) E 2 synthase(S)-1, an enzyme that catalyzes the isomerization of the cyclooxygenase (COX) product, PGH 2 , into PGE 2 , is a major source of PGE 2 in vivo . mPGES-1 deletion in mice was found to modulate experimentally evoked pain and inflammation and atherogenesis is retarded in mPGES-1 knockout (KO) mice. The impact of mPGES-1 deletion on formation of angiotensin II (Ang II)-induced abdominal aortic aneurysms (AAA) was studied in mice lacking the low density lipoprotein receptor (LDLR −/− ). AngII infusion increased aortic macrophage recruitment and nitrotyrosine staining while upregulating both mPGES-1 and COX-2 and urinary excretion of the major metabolite of PGE 2 (PGE-M). Deletion of mPGES-1 decreased both the incidence and severity of AAA and depressed excretion of both PGE-M and 8, 12-iso-iPF 2a -VI, which reflects lipid peroxidation in vivo . While Ang II infusion augmented prostaglandin biosynthesis, deletion of mPGES-1 resulted in rediversion to PGD 2 , reflected by its major urinary metabolite. However, deletion of the PGD 2 receptor, DP1, did not affect AAA in Ang II infused LDLR −/− mice. These observations indicate that deletion of mPGES-1 protects against AAA formation by AngII in hyperlipidemic mice, perhaps by decreasing oxidative stress. Inhibition of mPGES-1 may represent an effective treatment to limit aneurysm occurrence and expansion.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.116.suppl_16.II_108-d
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
    detail.hit.zdb_id: 1466401-X
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  • 10
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    Abstract 298: Microfibrillar Protein 4 is an Integrin avß3/5 Ligand Involved in Vascular Remodeling
    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: Arterial injury stimulates remodeling responses that, when overexuberant, leads to stenosis. This response is influenced by specific integrin signaling in vascular smooth muscle cells (VSMCs). Microfibrillar-associated protein 4 (MFAP4) is a matricellular integrin ligand localized to the vascular wall. We hypothesized that systemic MFAP4 (sMFAP4) associates to vascular remodeling processes and that MFAP4 enhances integrin dependent VSMC activation and vasculoproliferative disease-associated remodeling. We explored the hypotheses using a prospective human cohort with symptomatic obstructive peripheral arterial disease (PAD), VSMC culture studies, and produced MFAP4 deficient mice for studying neointima formation. We demonstrate that the highest tertile of sMFAP4 was significantly associated with primary patency after vascular reconstruction, and the overall need for vascular reconstruction and mortality in 343 PAD patients. MFAP4 mediated the adhesion, migration, and proliferation of VSMCs in an integrin αVβ3/5-dependent manner in vitro. These effects were inhibited by MFAP4-blocking antibodies. MFAP4-deficient mice displayed delayed neointimal formation when challenged with carotid artery ligation, but the compensatory outward remodeling of vessel diameter was reduced. In conclusion, sMFAP4 has the potential to serve as a systemic marker morbidity and mortality in PAD. MFAP4 regulates integrin αVβ3/5 signaling and pathological remodeling in vivo, and may have therapeutic implications in vasculoproliferative diseases.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/atvb.33.suppl_1.A298
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
    detail.hit.zdb_id: 1494427-3
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