Niacin reverses migratory macrophage foam cell arrest mediated by oxLDL in vitro.

Introduction: Niacin reduces vascular oxidative stress and down regulates inducible nitric oxide synthase, an enzyme mediating proatherosclerotic effects in part by increasing oxidative stress. Here, we evaluate whether Niacin reverses the redox sensitive migratory arrest of macrophages in response to oxidised(ox) LDL uptake.

Material And Methods: Migration of RAW264.

Outcome of giant cell arteritis of the arm arteries managed with medical treatment alone: cross-sectional follow-up study.

Objective: To assess the long-term outcome of GCA of the arm arteries under medical treatment alone.

Methods: Retrospective cross-sectional study of 34 patients with a diagnosis of GCA involving the arm arteries (i.e.

eNOS protects from atherosclerosis despite relevant superoxide production by the enzyme in apoE mice.

Background: All three nitric oxide synthase (NOS) isoforms are expressed in atherosclerotic plaques. NOS enzymes in general catalyse NO production. However, under conditions of substrate and cofactor deficiency, the enzyme directly catalyse superoxide formation.

Oxidative stress and compartment of gene expression determine proatherosclerotic effects of inducible nitric oxide synthase.

Genetic and pharmacological inhibition of inducible nitric oxide synthase (iNOS) decreases atherosclerosis development. Potential proatherogenic effects of iNOS include iNOS mediated oxidative stress and iNOS expression in different cellular compartments. Lesional iNOS can potentially produce nitric oxide radicals (NO), superoxide radicals (O2(-)), or both; these radicals may then react to form peroxynitrite.

Expression of neuronal nitric oxide synthase splice variants in atherosclerotic plaques of apoE knockout mice.

Objective: We previously reported that deletion of brain type neuronal nitric oxide synthase-alpha (nNOS-alpha) accelerates atherosclerosis in apolipoproteinE (apoE) knockout (ko) mice. The regulation of nNOS expression is complex, involving the generation of mRNA splice variants. The current study investigates occurrence and distribution of nNOS variants in atherosclerotic lesions of apoE ko and apoE/nNOS-alpha double ko (dko) animals.

Overlapping and distinct roles for PI3Kbeta and gamma isoforms in S1P-induced migration of human and mouse endothelial cells.

Aims: Sphingosine-1-phosphate (S1P), a key regulator of vascular homeostasis and angiogenesis, promotes endothelial cell migration via stimulation of phosphoinositide 3-kinase (PI3K). The aim of this study was to identify the role of PI3Kbeta and gamma isoforms and their downstream effector pathways in mediating endothelial cell migration induced by S1P.

Methods And Results: Experiments were performed in human umbilical vein endothelial cells (HUVEC) and murine lung endothelial cells (MLEC).

Ezetimibe potently reduces vascular inflammation and arteriosclerosis in eNOS-deficient ApoE ko mice.

Objective: Hypercholesterolemia is associated with decreased vascular nitric oxide bioavailability and deletion of endothelial nitric oxide synthase (eNOS) markedly accelerates atherosclerosis development in apolipoprotein E knockout (apoE ko) mice. The current study tests whether atheroprotection provided by a lipid lowering therapy with Ezetimibe depends on eNOS.

Methods/results: ApoE ko and apoE/eNOS double ko (dko) mice received a high fat diet with or without 0.

Large external iliac vein aneurysm in a patient with a post-traumatic femoral arteriovenous fistula.

We report about a young patient with a large aneurysm of the left external iliac vein associated with a traumatic arteriovenous fistula between the left superficial femoral artery and the femoral vein after a stab wound 20 years ago. The patient presented with swelling of the left leg, which developed during the past years and worsened after saphenectomy 12 months before hospital admission. The chronically hyperperfused common iliac artery proximal to the arteriovenous fistula was compressing the common iliac vein.

Native C-reactive protein induces endothelial dysfunction in ApoE-/- mice: implications for iNOS and reactive oxygen species.

Objective: In addition to being a risk marker for cardiovascular disease, recent data suggests that C-reactive protein (CRP) induces endothelial dysfunction and promotes oxidative stress. We evaluated the effects of two conformers of CRP (pentameric, or native [nCRP], versus monomeric, or modified [mCRP]) on vessel function and production of reactive oxygen species (ROS) in an in-vivo model of atherosclerosis.

Methods And Results: Female ApoE(-/-) mice, fed a "western-type" diet, were treated with either human nCRP or mCRP (2.

Tissue-specific effects of the nuclear factor kappaB subunit p50 on myocardial ischemia-reperfusion injury.

Nuclear factor kappaB (NF-kappaB) is a ubiquitous transcription factor activated by various stimuli implicated in ischemia-reperfusion injury. However, the role of NF-kappaB in cardiac ischemia-reperfusion injury has not yet been well defined. Therefore, we investigated reperfusion damage in mice with targeted deletion of the NF-kappaB subunit p50.

Atheroprotective effects of neuronal nitric oxide synthase in apolipoprotein e knockout mice.

Objective: All 3 isoforms of the nitric oxide synthase (NOS) are expressed in atherosclerotic lesions. To test whether neuronal NOS (nNOS) deficiency affects atherosclerosis, we studied apoE/nNOSalpha double knockout (DKO) and apolipoprotein E (apoE) knockout (KO) control mice.

Methods And Results: Lesion area was significantly increased in male DKO (66%) mice after 14 weeks and in female DKO animals (31%) after 24 weeks of "western" diet.

Integrin-linked kinase regulates endothelial cell survival and vascular development.

Integrin-linked kinase (ILK) is a phosphoinositide 3-kinase-dependent serine/threonine kinase that interacts with beta integrins. Here we show that endothelial cell (EC)-specific deletion of ILK in mice confers placental insufficiency with decreased labyrinthine vascularization, yielding no viable offspring. Deletion of ILK in zebra fish using antisense morpholino oligonucleotides results in marked patterning abnormalities of the vasculature and is similarly lethal.

Role of endothelial nitric oxide synthase in endothelial activation: insights from eNOS knockout endothelial cells.

The objective of this study was to determine whether absence of endothelial nitric oxide synthase (eNOS) affects the expression of cell surface adhesion molecules in endothelial cells. Murine lung endothelial cells (MLECs) were prepared by immunomagnetic bead selection from wild-type and eNOS knockout mice. Wild-type cells expressed eNOS, but eNOS knockout cells did not.