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  • 1
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    Online Resource
    Exploiting the Vascular Protective Effects of High-Density Lipoprotein and Its Apolipoproteins : An Idea Whose Time for Testing Is Coming, Part I
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Circulation Vol. 104, No. 19 ( 2001-11-06), p. 2376-2383
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 104, No. 19 ( 2001-11-06), p. 2376-2383
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/hc4401.098467
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
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  • 2
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    Effects of Recombinant Apolipoprotein A-I Milano on Aortic Atherosclerosis in Apolipoprotein E–Deficient Mice
    Ovid Technologies (Wolters Kluwer Health) ; 1998
    In:  Circulation Vol. 97, No. 8 ( 1998-03-03), p. 780-785
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 97, No. 8 ( 1998-03-03), p. 780-785
    Abstract: Background —We previously reported marked inhibitory effects of recombinant apolipoprotein (apo) A-I Milano /phospholipid complex (A-I Milano /PC) on neointimal lesions in balloon-injured iliofemoral arteries of hypercholesterolemic rabbits. In this study, we tested the hypothesis that apo A-I Milano /PC would inhibit aortic atherosclerosis in apo E–deficient mice. Methods and Results —Thirty-five apo E–deficient mice fed a high-cholesterol diet were included in the study. Control mice were killed at 20 (n=8) or 25 (n=7) weeks. Treated mice received 18 injections of either 40 mg/kg apo A-I Milano /PC (n=15) or PC only (n=5) intravenously every other day from 20 weeks until death at 25 weeks. Aortic atherosclerosis was identified with Sudan IV staining. Lipid and macrophage contents of the aortic sinus plaques were measured after oil-red O and Mac-1 antibody staining, respectively, and quantified with computed morphometry. In control mice, from 20 to 25 weeks, aortic atherosclerosis increased by 59% (11±1% versus 17±5% of the aortic surface, P =.002), and lipid content increased by 45% (22±8% versus 32±6% of plaque area, P =.02) without a significant change in macrophage content (10.8±2% versus 13.2±6%). Compared with 20-week-old untreated control mice, PC only–treated mice at 25 weeks demonstrated a 32% increase in aortic atherosclerosis (11±1% versus 15±4%, P =.01) and an increase in lipid content (22±8% versus 47±3%, P 〈 .0001) without a change in macrophage content (10.8±2% versus 11±2%). In comparison with 20-week-old untreated control mice, 25-week-old apo A-I Milano /PC–treated mice demonstrated no increase in aortic atherosclerosis (11±1% versus 10±4%, P =NS), a 40% reduction in lipid content (22±8% versus 13±8%, P =.01), and a 46% reduction in macrophage content (10.8±2% versus 5.8±2.9%; P =.03). Serum cholesterol levels were markedly elevated in all groups and did not change significantly with apo A-I Milano /PC or PC only. In vitro, apo A-I Milano /PC stimulated cholesterol efflux from cholesterol-loaded FU5AH hepatoma cell lines in a dose-dependent manner, whereas PC only or PC-free apo A-I Milano had no effect. Conclusions —Recombinant A-I Milano /PC prevented progression of aortic atherosclerosis and reduced lipid and macrophage content of plaques in apo E–deficient mice despite severe hypercholesterolemia. Thus, A-I Milano /PC may have a role in inhibiting progression and promoting stabilization of atherosclerosis.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.97.8.780
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1998
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  • 3
    Online Resource
    Online Resource
    Acute Myocardial Infarction in Human Immunodeficiency Virus–Infected Patients
    American Medical Association (AMA) ; 2003
    In:  Archives of Internal Medicine Vol. 163, No. 4 ( 2003-02-24), p. 457-
    Details
    In: Archives of Internal Medicine, American Medical Association (AMA), Vol. 163, No. 4 ( 2003-02-24), p. 457-
    Type of Medium: Online Resource
    ISSN: 0003-9926
    URL: Article
    DOI: 10.1001/archinte.163.4.457
    RVK:
    XA 29200
    Language: English
    Publisher: American Medical Association (AMA)
    Publication Date: 2003
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  • 4
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    Membrane Type 1 Matrix Metalloproteinase Expression in Human Atherosclerotic Plaques : Evidence for Activation by Proinflammatory Mediators
    Ovid Technologies (Wolters Kluwer Health) ; 1999
    In:  Circulation Vol. 99, No. 24 ( 1999-06-22), p. 3103-3109
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 99, No. 24 ( 1999-06-22), p. 3103-3109
    Abstract: Background —Matrix metalloproteinases (MMPs) are expressed in atherosclerotic plaques, where in their active form, they may contribute to vascular remodeling and plaque disruption. In this study, we tested the hypothesis that membrane type 1 MMP (MT1-MMP), a novel transmembrane MMP that activates pro-MMP-2 (gelatinase A), is expressed in human atherosclerotic plaques and that its expression is regulated by proinflammatory molecules. Methods and Results —MT1-MMP expression was examined in normal and atherosclerotic human arteries by immunocytochemistry with specific antibodies. MT1-MMP expression in human saphenous vein–derived smooth muscle cells (SMCs) maintained in tissue culture was determined under basal conditions and in response to proinflammatory molecules (interleukin [IL]-1α, tumor necrosis factor [TNF] -α, and oxidized LDL [ox-LDL]) by use of Northern blot and ribonuclease protection assays for mRNA, Western blot and immunoprecipitation for protein, and gelatin zymography for catalytic activity. Medial SMCs of normal vessel wall expressed MT1-MMP. In atherosclerotic arteries, MT1-MMP expression was noted within the complex atheroma colocalizing with SMCs and macrophages (Mφ). Cultured SMCs constitutively expressed MT1-MMP mRNA and protein, which increased 2- to 4-fold over control in a time-dependent manner within 4 to 8 hours of exposure to IL-1α, TNF-α, and ox-LDL (thiobarbituric acid–reactive substances, 13.4 nmol/mg LDL protein), whereas native LDL had no effect. Flow cytometry revealed MT1-MMP expression by human monocyte-derived Mφ, which increased 3.8-fold over baseline within 6 hours after exposure to 10 ng/mL TNF-α. Conclusions —This study demonstrates that MT1-MMP, an activator of pro-MMP-2, is expressed by SMCs and Mφ in human atherosclerotic plaques. Furthermore, proinflammatory molecules upregulate MT1-MMP expression in vascular SMCs and Mφ. Thus, activation of SMCs and Mφ by proinflammatory molecules may influence extracellular matrix remodeling in atherosclerosis by regulating MT1-MMP expression.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.99.24.3103
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1999
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  • 5
    Online Resource
    Online Resource
    High-Dose Recombinant Apolipoprotein A-I Milano Mobilizes Tissue Cholesterol and Rapidly Reduces Plaque Lipid and Macrophage Content in Apolipoprotein E–Deficient Mice : Potential Implications for Acute Plaque Stabilization
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Circulation Vol. 103, No. 25 ( 2001-06-26), p. 3047-3050
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 103, No. 25 ( 2001-06-26), p. 3047-3050
    Abstract: Background —Repeated doses of recombinant apolipoprotein A-I Milano phospholipid complex (apoA-I m ) reduce atherosclerosis and favorably change plaque composition in rabbits and mice. In this study, we tested whether a single high dose of recombinant apoA-I m could rapidly mobilize tissue cholesterol and reduce plaque lipid and macrophage content in apoE-deficient mice. Methods and Results —High cholesterol–fed, 26-week-old apoE-deficient mice received a single intravenous injection of saline (n=16), 1080 mg/kg dipalmitoylphosphatidylcholine (DPPC; n=14), or 400 mg/kg of recombinant apoA-I m complexed with DPPC (1:2.7 weight ratio; n=18). Blood was sampled before and 1 and 48 hours after injection, and aortic root plaques were evaluated for lipid content and macrophage content after oil-red O and immunostaining, respectively. One hour after injection, the plasma cholesterol efflux–promoting capacity was nearly 2-fold higher in recombinant apoA-I m –treated mice compared with saline and DPPC-treated mice ( P 〈 0.01). Compared with baseline values, serum free cholesterol, an index of tissue cholesterol mobilization, increased 1.6-fold by 1 hour after recombinant apoA-I m injection, and it remained significantly elevated at 48 hours ( P 〈 0.01). Mice receiving recombinant apoA-I m had 40% to 50% lower lipid content ( P 〈 0.01) and 29% to 36% lower macrophage content ( P 〈 0.05) in their plaques compared with the saline- and DPPC-treated mice, respectively. Conclusions —A single high dose of recombinant apoA-I m rapidly mobilizes tissue cholesterol and reduces plaque lipid and macrophage content in apoE-deficient mice. These findings suggest that this strategy could rapidly change plaque composition toward a more stable phenotype.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/hc2501.092494
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
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  • 6
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    Online Resource
    Therapeutic Concentrations of Heparin Augment Platelet Activation at the Time of Coronary Angiography
    SAGE Publications ; 1998
    In:  Journal of Cardiovascular Pharmacology and Therapeutics Vol. 3, No. 2 ( 1998-06), p. 91-101
    Details
    In: Journal of Cardiovascular Pharmacology and Therapeutics, SAGE Publications, Vol. 3, No. 2 ( 1998-06), p. 91-101
    Abstract: Background: Besides its anticoagulant effects, heparin is known to alter platelet (PLT) function. We examined the effects of unfractionated heparin on PLT function in patients with stable coronary artery disease (CAD). Methods and Results: PLT function was evaluated by whole-blood flow cytometry to detect PLT CD62 expression and by impedance aggregometry to assess platelet aggregation (PA) before and after bolus intravenous administration of low-dose heparin (2713 ± 1231 U) in 16 patients undergoing coronary angiography (group 1) and high-dose heparin (7937 ± 2414 U) in 16 patients undergoing coronary angioplasty (group 2). Activated clotting time (ACT) and plasma antifactor-Xa heparin levels also were measured. Heparin increased PLT CD62 expression, which was significantly more pronounced in group 1 patients with plasma heparin levels less than 0.7 U/mL and ACT of 222 ± 52 seconds compared with group 2 patients with heparin levels greater than 0.7 U/mL and ACT of 365 ± 86 seconds (8 ± 9 v -1 ± 4% change in resting PLTs, P = .01, and 11 ± 12 v 1 ± 6% increase in adenosine diphosphate (ADP) [5 μM]-stimulated PLTs, P = .02). Heparin produced a slight increase in PA in group 1 patients (1.4 ± 5.3 ohms) as compared with the group 2 patients, where it significantly suppressed PA (-3.0 ± 5.3 ohms, P 〈 .05 v group 1). A strong and statistically significant negative correlation between change in platelet CD62 expression and heparin concentration was observed in group 1 patients ( r = -.5, P = .05, —ADP; r = —.65, P = .006, +ADP), whereas this relationship was weak and did not reach statistical significance in group 2 patients ( r = -0.4, P = .2, -ADP; r = .11, P = 0.9; +ADP). Conclusion: Bolus administration of intravenous heparin augmented PLT activation in patients at clinically relevant anticoagulant concentrations ( 〈 0.7 U/mL). These findings may have implications for optimal dosing strategy for heparin as an antithrombotic agent in clinical situations characterized by platelet-dependent thrombotic events.
    Type of Medium: Online Resource
    ISSN: 1074-2484 , 1940-4034
    URL: Article
    DOI: 10.1177/107424849800300201
    Language: English
    Publisher: SAGE Publications
    Publication Date: 1998
    detail.hit.zdb_id: 2230155-0
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  • 7
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    Online Resource
    Differentiation of adherent human monocytes into macrophages markedly enhances tissue factor protein expression and procoagulant activity
    Elsevier BV ; 2002
    In:  Atherosclerosis Vol. 161, No. 1 ( 2002-3), p. 35-43
    Details
    In: Atherosclerosis, Elsevier BV, Vol. 161, No. 1 ( 2002-3), p. 35-43
    Type of Medium: Online Resource
    ISSN: 0021-9150
    URL: Article
    DOI: 10.1016/S0021-9150(01)00616-5
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2002
    detail.hit.zdb_id: 1499887-7
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  • 8
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    Online Resource
    Decreased Neointimal Thickening After Arterial Wall Injury in Inducible Nitric Oxide Synthase Knockout Mice
    Ovid Technologies (Wolters Kluwer Health) ; 1999
    In:  Circulation Research Vol. 85, No. 12 ( 1999-12-03), p. 1192-1198
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 85, No. 12 ( 1999-12-03), p. 1192-1198
    Abstract: Abstract —Mechanical injury in vivo results in the expression of the inducible form of nitric oxide synthase (iNOS) in vascular smooth muscle cells. However, the role of iNOS in modulating neointima formation after arterial wall injury is not clear. To determine whether the induction of iNOS gene expression promotes or attenuates the neointimal response to injury, we used a murine model of perivascular injury induced by placing a periadventitial collar around the carotid arteries in both wild-type and iNOS knockout mice (iNOS-KO mice). Periadventitial injury induced iNOS expression in the wild-type but not the iNOS-KO mice. Neointimal area and the intima/media ratio were significantly less in the iNOS-KO mice compared with the wild-type mice at 21 days. Injury-induced proliferation of medial cells and vascular cell adhesion molecule-1 expression were also attenuated in iNOS-KO mice compared with wild-type mice. The induction of iNOS and the activation of the nuclear factor-κB–mediated pathway were also demonstrated in an in vitro injury model. We conclude that mechanical injury in vivo and in vitro induces iNOS expression and that lack of iNOS expression attenuates neointima formation after perivascular arterial injury. Taken together, these findings suggest that iNOS expression after vascular injury may promote neointima formation.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.85.12.1192
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1999
    detail.hit.zdb_id: 1467838-X
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  • 9
    Online Resource
    Online Resource
    Effect of Exposure to Cigarette Smoke on Carotid Artery Intimal Thickening : The Role of Inducible NO Synthase
    Ovid Technologies (Wolters Kluwer Health) ; 2004
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 24, No. 9 ( 2004-09), p. 1652-1658
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 24, No. 9 ( 2004-09), p. 1652-1658
    Abstract: We investigated the role of inducible nitric oxide synthase (iNOS) in intimal thickening with exposure to cigarette smoke (CS) exposure in WT mice was associated with increased arterial iNOS expression, superoxide production, AP-1 activation, serum NO, and intimal thickening. Inhibition or deletion of iNOS abrogated the effects of CS.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/01.ATV.0000139925.84444.ad
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2004
    detail.hit.zdb_id: 1494427-3
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  • 10
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    Intravenous Magnesium in Experimental Stent Thrombosis in Swine
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 21, No. 9 ( 2001-09), p. 1544-1549
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 21, No. 9 ( 2001-09), p. 1544-1549
    Abstract: We investigated the effects of magnesium on acute platelet-dependent stent thrombosis in an ex vivo porcine arteriovenous shunt model of high-shear blood flow. Control nitinol stents were expanded to 2 mm in diameter in a tubular perfusion chamber interposed in the shunt and exposed to flowing arterial blood at a shear rate of 2100 s −1 for 20 minutes (n=156 perfusion runs in 10 swine). Animals were treated with intravenous heparin or MgSO 4 alone (2 g bolus over 20 minutes, followed by 2 g/h infusion) and combined heparin plus MgSO 4 in random fashion. Effects on thrombus weight (TW), platelet aggregation, bleeding time, activated clotting time, mean arterial blood pressure, and heart rate were quantified. Data points in the magnesium-treated animals were examined within 20 minutes after bolus (Mg-early) and 〉 40 minutes after bolus (Mg-late). Stent TW (20±3 mg, pretreatment) was reduced by 42±21%, 47±19%, 48±16%, 67±12%, and 86±8% in the groups treated with Mg-early alone, Mg-late alone, heparin alone, heparin+Mg-early, and heparin+Mg-late, respectively (all P 〈 0.001 versus pretreatment, P 〈 0.001 for heparin+Mg-early and Mg-late versus heparin or magnesium alone, and P 〈 0.05 for heparin+Mg-late versus heparin+Mg-early, ANOVA). Magnesium had no significant effect on platelet aggregation, activated clotting time, or bleeding time. There were no significant effects on heart rate or mean arterial blood pressure. The serum magnesium level was inversely correlated with TW ( r =−0.70, P =0.002). In conclusion, treatment with intravenous MgSO 4 produced a time-dependent inhibition of acute stent thrombosis under high-shear flow conditions without any hemostatic or significant hemodynamic complications. Thus, magnesium may be an effective agent for preventing stent thrombosis.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/hq0901.094493
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
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