Accelerated migration and proliferation of smooth muscle cells cultured from neointima induced by a vena cava filter.

Formation of a neointima is associated with grafted artery or vein, angioplasty, and stent and inferior vena cava filter (IVCF) implantation. Contributing to the neointima is a population of vascular smooth muscle cells (SMC) that migrates from media and subsequently proliferates within intima. The purpose of this present study was to culture SMC from normal vessel wall and from neointima and to compare migration and growth of these cells.

Regulation of human vascular smooth muscle cell migration by beta-adrenergic receptors.

Migration and proliferation of vascular smooth muscle cells (VSMCs) are two events involved in atherosclerosis, restenosis after balloon angioplasty, and stenosis of grafted vessels. Platelet-derived growth factor (PDGF) found in stenotic vessels is known to induce migration of VSMCs. VSMCs express both alpha- and beta-adrenergic receptors on their surface, and blood vessels are innervated by the adrenergic nervous system and exposed to circulating epinephrine.

Removal of the OptEase retrievable vena cava filter is not feasible after extended time periods because of filter protrusion through the vena cava.

Background: Therapeutic and prophylactic vena cava filters (VCFs) are used to prevent pulmonary embolism. Concerns exist over placing a permanent filter in a young trauma patient. Recently, retrievable VCFs have become available.

Two distinct phenotypes of rat vascular smooth muscle cells: growth rate and Production of tumor necrosis factor-alpha.

The monoclonal theory of atherosclerosis postulates that a subpopulation of vascular smooth muscle cells (VSMCs) is selectively expanded in response to pathologic stimuli and accumulates in vascular intima. The purpose of this research was to clone VSMC, determine growth rates of the clones and their ability to release the mitogenic cytokine tumor necrosis factor-alpha (TNF-alpha). With approval of the institutional animal care and use committee, VSMCs were isolated and cultured from the thoracic aortas of three rats.

Angiotensin II induces proliferation of human cerebral artery smooth muscle cells through a basic fibroblast growth factor (bFGF) dependent mechanism.

Remodeling of cerebral arteries in hypertension produces thickened vessel walls associated with atherosclerotic plaque formation. In both thickening and plaque formation, proliferation of vascular smooth muscle cells is a hallmark. Genetically hypertensive rats treated with an angiotensin II (Ang II) AT1 receptor antagonist inhibited thickening of cerebral arteries suggesting a mitogenic action of Ang II on cerebral arterial VSMC (CVSMC).

Regulation of tumor necrosis factor-alpha production in the isolated rat heart stimulated by bacterial lipopolysaccharide or reactive oxygen.

Reperfusion after cardiopulmonary bypass causes induction of reactive oxygen species (ROS), elevated plasma levels of bacterial lipopolysaccharide (LPS), and production of tumor necrosis factor-alpha (TNF) by the heart. Nuclear factor-kappaB (NF-kappaB) regulates the expression of TNF. Because NF-kappaB is activated by both LPS and ROS, we hypothesized that an inhibitor of NF-kappaB, pyrrolidine dithiocarbamate (PDTC), would block release of TNF from the heart stimulated by these two agents.

TNF-alpha induces proliferation or apoptosis in human saphenous vein smooth muscle cells depending on phenotype.

Tumor necrosis factor (TNF)-alpha is implicated in development of restenotic and atherosclerotic vascular lesions, which are pathological processes involving both proliferation and apoptosis of vascular smooth muscle cells (VSMCs). Human VSMCs were recently found to contain heterogeneous subpopulations. We therefore examined whether TNF has different effects on distinct subpopulations of VSMCs.

Rapamycin inhibits release of tumor necrosis factor-alpha from human vascular smooth muscle cells.

Neointimal proliferation with plaque formation is the principal cause of coronary artery disease. In the neointima, inflammatory cytokines like tumor necrosis factor-alpha (TNF-alpha) are expressed by vascular smooth muscle cells (VSMCs). These cytokines stimulate proliferation and migration of VSMCs, events that are crucial to neointima formation.

Reactive oxygen species-sensitive p38 MAPK controls thrombin-induced migration of vascular smooth muscle cells.

Thrombin has been implicated in the development of atherosclerosis and restenosis, in which migration of vascular smooth muscle cells (VSMC) is a crucial event. Thrombin-stimulated VSMC migration is associated with increased generation of reactive oxygen species (ROS), activation of mitogen-activated protein kinases (MAPKs), and production of growth factors and chemoattractants. In this study, we examined the interrelation of these signals to determine the pathway controlling thrombin-directed migration of human VSMC.

Phenotypic diversity of smooth muscle cells isolated from human intracranial basilar artery.

The present work examined heterogeneity of vascular smooth muscle cells cultured from human cerebral arteries that has not been previously reported. Primary smooth muscle cell cultures were isolated from human intracranial basilar arteries. Using a ring isolation method, multiple clones were generated from the cell cultures.

Smooth muscle cell migration stimulated by interleukin 6 is associated with cytoskeletal reorganization.

Background: Interleukin 6 (IL-6) is elevated in the arterial wall in atherosclerosis and restenosis after angioplasty. An important contributor to these pathologies is migration of vascular smooth muscle cells (VSMC), which is often associated with cytoskeletal reorganization initiated by growth factors and chemokines. We recently reported that IL-6 stimulated migration of VSMC.

A method to isolate morphologically distinct clones of smooth muscle cells from human saphenous vein.

The monoclonal theory of atherosclerosis postulates that a certain subpopulation of vascular smooth muscle cells (VSMC) is selectively expanded in response to pathological stimuli thereby contributing to the formation of atherosclerotic plaques. VSMC cloning experiments will be important in characterizing the phenotypic composition of VSMC in atherosclerotic plaques. However, the difficulty in cloning human VSMC is well recognized.

Bacterial lipopolysaccharide-stimulated release of tumor necrosis factor-alpha from the isolated rat heart: the effect of aprotinin and forskolin.

Aprotinin has been reported to reduce plasma levels of inflammatory cytokines associated with cardiopulmonary bypass (CPB). Because CPB is also associated with elevated levels of bacterial lipopolysaccharide (LPS) and LPS stimulates release of inflammatory cytokines from the heart we tested the hypothesis that aprotinin would inhibit cardiac release of tumor necrosis factor-alpha (TNF) provoked by LPS. Isolated rat hearts were perfused Langendorf style.

Cyclic AMP inhibits production of interleukin-6 and migration in human vascular smooth muscle cells.

Background: Gene expression induced by tumor necrosis factor-alpha (TNF-alpha) is involved in the regulation of vascular smooth muscle cell (VSMC) proliferation and migration, two events critical to formation of stenotic vascular lesions. In some systems, elevating adenosine 3',5'-cyclic monophosphate (cyclic AMP) inhibits TNF-alpha induced gene transcription. We recently demonstrated that interleukin-6 (IL-6) was chemotactic to VSMC.

Isoproterenol inhibits transcription of cardiac cytokine genes induced by reactive oxygen intermediates.

Background: Cytokines such as tumor necrosis factor alpha (TNF-alpha) are produced by the myocardium in heart disease and might be stimulated by reactive oxygen. In some cell types, cyclic adenosine monophosphate (AMP) inhibits TNF-alpha production. The authors tested the hypothesis that stimulation of cardiac beta-adrenergic receptors would inhibit cytokine gene transcription induced by reactive oxygen.

An IkappaB-alpha mutant inhibits cytokine gene expression and proliferation in human vascular smooth muscle cells.

Background: Inflammatory reaction and intimal proliferation of smooth muscle cells are characteristics of vascular stenotic lesions. Nuclear factor kappaB (NF-kappaB) is involved in regulation of inflammation and cell survival in a variety of cell types. We tested a hypothesis that selective inhibition of NF-kappaB by expression of a mutated, nondegradable inhibitor of NF-kappaB, IkappaB-alphaM, would inhibit proinflammatory cytokine expression and proliferation in human vascular smooth muscle cell.