Journal of Vascular Research (J VASC RES)
The ëJournal of Vascular Researchí publishes original articles and reviews of scientific excellence in vascular biology, physiology and pathophysiology. The scope of the journal covers a broad spectrum of vascular and lymphatic research including vascular structure, vascular function, hemodynamics, mechanics, cell signalling, intercellular communication, growth and differentiation. Papers employing cellular, biophysical and molecular techniques, as well as more classical approaches are welcome. Manuscript processing times are, consistent with stringent review, held to 5ñ6 weeks for the first decision, and 3ñ4 weeks for Rapid Communications. Publication time from date of acceptance should be no more than 5 months, and shorter for Rapid Communications and Correspondence
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Other titlesJournal of vascular research (Online)
Material typeDocument, Periodical, Internet resource
Document typeInternet Resource, Computer File, Journal / Magazine / Newspaper
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Publications in this journal
Article: Morphological and Functional Alterations in the Aorta of the Chronically Hypoxic Fetal Rat.Journal of Vascular Research 01/2011; 49:50-58.
Article: Saxatilin, a snake venom disintegrin, regulates platelet activation associated with human vascular endothelial cell migration and invasion.[show abstract] [hide abstract]
ABSTRACT: Platelet activation results in platelet aggregation and the secretion of granules, which contain a variety of constituents including nonprotein molecules, adhesive proteins and hydrolases. The platelet-derived supernatant (PDS), which contains these granules, is known to trigger the activation of endothelium and chemotaxis of monocytes. PDS derived from collagen-activated platelets stimulated human umbilical vein endothelial cell (HUVEC) migration and invasion, as measured through the use of a Boyden chamber. This collagen-induced PDS also triggered integrin alpha(v)beta(3) upregulation in HUVECs. The inclusion of a neutralizing antibody to platelet-derived growth factor (PDGF)-B abolished HUVEC migration/invasion and integrin alpha(v)beta(3) upregulation, showing that PDGF-AB mediates the proangiogenic effects of collagen-activated PDS. Saxatilin, a snake venom disintegrin known to interrupt platelet aggregation by antagonizing integrin alpha(IIb)beta(3), inhibited the collagen-induced platelet activation and abolished the angiogenic properties of PDS. Saxatilin also inhibited the collagen-induced phosphorylation of Syk, a key mediator of inside-out signaling in platelet activation. Saxatilin inhibits platelet activation, platelet PDGF-AB release as well as subsequent endothelial cell migration and invasion.Journal of Vascular Research 02/2007; 44(2):129-37.
Article: Production of inflammatory molecules in peripheral blood mononuclear cells from severely glucose-6-phosphate dehydrogenase-deficient subjects.[show abstract] [hide abstract]
ABSTRACT: We have previously demonstrated that Mediterranean glucose-6-phosphate dehydrogenase (G6PD)-deficient peripheral blood mononuclear cells (PBMC) respond to mitogenic stimuli with a reduced cholesterol synthesis and growth. In the present study, we have investigated the release of inflammatory molecules by PBMC following a mitogenic stimulus, as well as the transformation to foam cells of monocyte-derived macrophages from severely G6PD-deficient and normal subjects. PBMC from G6PD-deficient subjects produced interleukin (IL)-1beta and IL-6 to a lower extent compared with normal subjects. 5-Hydroxyeicosatetraenoic acid, a primary product of 5-lipoxygenase, was slightly decreased. Tumour necrosis factor-alpha and IL-1beta secretion was significantly reduced in monocyte-derived macrophages. No difference was found in IL-10 secretion, whereas transforming growth factor-beta was invariably found to be significantly higher in G6PD-deficient cells. In cells incubated with acetylated low-density lipoprotein, cholesterol esterification and its storage in lipid droplets were lower than in normal G6PD cells. We conclude that by reducing the secretion of inflammatory molecules by PBMC and increasing the secretion of transforming growth factor-beta and the capability of monocyte-derived macrophages to accumulate lipid droplets and convert into foam cells, G6PD deficiency may confer a partial protection against atherosclerosis leading to the reduced risk of cardiovascular diseases reported in G6PD-deficient subjects.Journal of Vascular Research 02/2007; 44(4):253-63.
Article: Effect of dietary chromium on resistance artery function and nitric oxide signaling in the sucrose-fed spontaneously hypertensive rat.[show abstract] [hide abstract]
ABSTRACT: Consumption of high-glycemic index foods contributes to the development of hypertension in some patients. Likewise, in spontaneously hypertensive rats (SHR), high sucrose promotes a secondary rise in systolic blood pressure (SBP). Chromium (III) (Cr(3+)) prevents sucrose-induced hypertension, but leaves the basal hypertension that characterizes SHR intact. Since hypertension entails increased peripheral resistance, we compared effects of Cr(3+) on resistance arteries from SHR fed low-glycemic (starch) versus high-glycemic (sucrose) index diets. Subgroups of SHR also received Cr(3+). Structure, stiffness, and vasodilation of mesenteric resistance arteries were studied using pressurized myography. Sucrose increased SBP in SHR and, exclusively in sucrose-fed SHR, Cr(3+) reduced SBP and augmented acetylcholine or nitroprusside-dependent vasodilation. Neither sucrose nor Cr(3+) affected artery structure or stiffness. Since Cr(3+) enhanced vasodilation, we assessed endothelial NO synthase (eNOS), guanylate cyclase, cGMP-dependent protein kinase (PKG-1alpha and 1beta), and PKG activity by immunoblotting. Sucrose reduced eNOS, PKG-1beta, and PKG activity. Cr(3+) prevented the effects of sucrose on NO signaling. In hypertension exacerbated by high-glycemic index diet, Cr(3+) reduces SBP. The BP-lowering effect of Cr(3+), selectively on sucrose-induced but not basal hypertension in SHR, involves at least in part, improving vasodilatory function vis-à-vis restoration of NO signaling in resistance arteries.Journal of Vascular Research 02/2007; 44(2):110-8.
Article: Taurine attenuates acute hyperglycaemia-induced endothelial cell apoptosis, leucocyte-endothelial cell interactions and cardiac dysfunction.[show abstract] [hide abstract]
ABSTRACT: Hyperglycaemia is implicated in microvascular inflammatory injury and subsequent cardiac injury/dysfunction. Leucocyte adhesion to the endothelium, migration into tissue and toxic metabolite release are early critical steps. Taurine is a semi-essential amino acid that is endothelial protective and restrains excess leucocyte activity by the formation of less toxic inflammatory mediators. The aim was to establish if taurine reduces acute hyperglycaemia-induced endothelial cell apoptosis and leucocyte interactions and associated cardiac abnormalities. Male Sprague-Dawley rats (190-250 g) were randomised to control, hyperglycaemia, and hyperglycaemia plus taurine pre-treated groups. Taurine was gavaged (200 mg/kg body weight) for 5 days. Intravenous hyperglycaemia was established which was 4 times that of baseline for the 3-hour experiment. Using intravital microscopy, mesenteric post-capillary venules were examined for leucocyte rolling, adhesion and migration every 30 min from baseline. Endothelial cell apoptosis and intracellular adhesion molecule (ICAM-1) expression were assessed. In a separate experiment, blood pressure, pulse rate, cardiac injury marker (troponin T), cardiac tissue injury and oedema were also assessed. Hyperglycaemia significantly increased leucocyte adhesion and migration. Blood pressure and troponin T were also elevated significantly. Taurine prevented these cardiac changes, endothelial cell apoptosis and ICAM-1 expression. Taurine may have a therapeutic role in reducing diabetic microvascular inflammatory injury and concomitant cardiac dysfunction.Journal of Vascular Research 02/2007; 44(1):31-9.
Article: The effects of endothelial factor inhibition on the time course of responses of isolated rat coronary arteries to intraluminal flow.[show abstract] [hide abstract]
ABSTRACT: The aims of this study were to investigate, for the first time, the effects of endothelial factor inhibition on both the magnitude and dynamics of the response of isolated small coronary arteries to intraluminal flow. Isolated rat coronary arteries were mounted on a pressure myograph and left to develop myogenic tone. Flow was introduced and maintained until stable diameters were attained. Dilatory responses were observed which were maximal at low flow rates (5-10 microl/min) and thus shear stresses (1-2 dyn/cm(2)). These responses were transient in nature. Transient dilations were also observed upon cessation of flow. All responses (to 5 microl/min) were endothelium dependent and were completely abolished by addition of charybdotoxin (100 nM) and apamin (100-500 nM) suggesting an important role for a hyperpolarizing mechanism most likely involving an endothelium-derived hyperpolarizing factor. However, inhibitors of nitric oxide synthase (L-NNA; 100 microM) or cyclo-oxygenase (indomethacin; 10 microM) also modulated the response causing an increase and decrease in maximum vasodilation, respectively. By examining the time course we showed that both agents also made the response significantly more transient in nature. These results show that inhibition of endothelial factor pathways can influence both the magnitude and dynamics of the response of isolated rat coronary arteries to flow.Journal of Vascular Research 02/2007; 44(3):223-33.
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ABSTRACT: Although the etiology of venous insufficiency is not well understood, immune response and aging are beginning to emerge as contributing factors. Factors involved in tissue remodeling such as TGF-beta(1) also seem to play an important role in extracellular matrix production. The aim of this study was to explore the relationship between chronic venous insufficiency and TGF-beta(1) examining the latent/mature form of TGF-beta(1) and the presence of mast cells. Effects of age were also evaluated. Saphenous veins were obtained from patients subjected to aortocoronary bypass (controls) and undergoing varicose vein surgery. These were immunolabeled using anti-LAP TGF-beta(1)/anti-TGF-beta(1) antibodies and subjected to Western blot. Mast cell population was identified by metachromatic staining. Latent TGF-beta(1) was significantly reduced in varicose veins from older subjects. In contrast, smooth muscle cells obtained from the varicosities showed intense levels. Mature TGF-beta(1) significantly differed between healthy and varicose veins. No mature TGF-beta(1) was detected in the cell cultures. Mast cell number and degranulation were increased with aging and varicose disease, colocalizing with the mature form of TGF-beta(1). Aging and varicose pathology induce dysregulation of TGF-beta(1) that could play an important role in the fibrous process, representing the final stages of venous insufficiency.Journal of Vascular Research 02/2007; 44(3):192-201.
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ABSTRACT: The detailed spatial arrangement of the vasa vasorum (VV) of the human great saphenous vein (HGSV) was demonstrated in qualitative and quantitative terms. Segments of the HGSV taken from cadavers 12-24 h post mortem and from patients undergoing aortocoronary bypassing were studied by light microscopy of India-ink-injected specimens and by scanning electron microscopy of vascular corrosion casts. Arterial feeders were found to approach the HGSV from nearby arteries every 15 mm forming a rich capillary network within the adventitia and the outer two thirds of the media in normal HGSV, while in HGSV with intimal hyperplasia capillary meshes extended into the inner layers of the media. Within the media, capillary meshes ran circularly. Postcapillary venules drained centrifugally towards the adventitial venous vessels which finally formed venous drainers running adjacent to the arterial feeders. Three-dimensional morphometry of vascular corrosion casts of VV revealed that diameters of (i) arterial VV ranged from 11.6 to 36.6 microm, (ii) capillary VV from 4.7 to 11.6 microm and (iii) venous VV ranged from 11.6 to 200.3 microm. The 3D network of VV suggests these layers are metabolically highly active and therefore require a continuous blood supply. We conclude, therefore, that the VV network must be preserved during in situ bypassing.Journal of Vascular Research 02/2007; 44(2):157-66.
Article: Impaired release of bioactive parathyroid hormone-related peptide in patients with pulmonary hypertension and endothelial dysfunction.[show abstract] [hide abstract]
ABSTRACT: Parathyroid hormone-related protein (PTHrP) is an endothelial-derived vasoactive peptide. This study investigated whether bioactive PTHrP is locally released in a pressure-dependent way. A PTHrP antibody directed against the midregional part of PTHrP was used to analyze PTHrP in plasma samples. The biological activity of this PTHrP-like peptide was investigated in vitro. Plasma values were determined in samples from the left pulmonary artery and the arteria femoralis, taken under basal conditions and after the application of oxygen or iloprost to lower the pulmonary pressure. Twenty young patients (mean age 6.5 years), who were catheterized for an analysis of the reactivity of the pulmonary bed, were investigated. Endothelial function was investigated by acetylcholine responsiveness. The antibody recognized a 30-kDa protein with in vitro PTHrP-like activity. In 11 patients (responders) with intact endothelial function, the PTHrP values determined in the left pulmonary artery were higher than those in the arteria femoralis. The local increase in the PTHrP concentration was reduced when either oxygen or iloprost lowered the pressure. Nine patients with endothelial dysfunction did not show any concentration gradients at any time (nonresponders). The local concentration of bioactive PTHrP is increased in patients with pulmonary hypertension and normal endothelial function.Journal of Vascular Research 02/2007; 44(1):67-74.
Article: Neuregulin-1 attenuates neointimal formation following vascular injury and inhibits the proliferation of vascular smooth muscle cells.[show abstract] [hide abstract]
ABSTRACT: Neuregulin-1 (NRG-1) is expressed in vascular endothelial cells, and its receptors are localized to the underlying smooth muscle cells. However, the role of NRG-1 in vascular function and injury is largely unknown. First, the expression of NRG-1 and its receptors (erbB receptors) was analyzed after balloon injury to the rat carotid artery. NRG-1 and erbB expression levels were low in uninjured vessels; however, NRG-1 and erbB4 were upregulated following injury. We then examined the effect of NRG-1 on neointimal formation following balloon injury. NRG-1 was administered by tail-vein injection prior to injury and every 2 days following injury. Two weeks after injury, NRG-1-treated animals demonstrated a 50% reduction in lesion size compared with controls receiving the vehicle. To examine possible mechanisms for NRG-1 action, we examined its effects on vascular smooth muscle cell (VSMC) function. Rat VSMC cultures were pretreated with NRG-1 for 24 h and then stimulated with platelet-derived growth factor. NRG-1 significantly decreased platelet-derived growth factor-stimulated VSMC proliferation and migration. These findings suggest that NRG-1 may be a novel therapeutic candidate for the treatment of restenosis and atherosclerosis.Journal of Vascular Research 02/2007; 44(4):303-12.
Article: Transglutaminase 1 stabilizes beta-actin in endothelial cells correlating with a stabilization of intercellular junctions.[show abstract] [hide abstract]
ABSTRACT: Microvascular endothelial monolayers from mouse myocardium become resistant to various barrier-compromising stimuli correlating with the expression of transglutaminase 1 (TGase1) and its translocation towards cellular junctions. In contrast, endothelial monolayers from mouse lung microvessels do not express TGase1 and remain sensitive to barrier-compromising stimuli corresponding to the known in vivo sensitivity of the lung microvasculature. Using the TGase-substrate 5-(biotinamido)-pentylamine, specific TGase inhibitors and RNAi, one target protein of TGase1 in endothelial cells was found to be beta-actin, suggesting that tissue-specific stabilization of the cortical actin filament network by intracellular TGase1 activity may play a role in controlling barrier properties of endothelial monolayers.Journal of Vascular Research 02/2007; 44(3):234-40.
Article: Vitamin D analogs modulate the expression of plasminogen activator inhibitor-1, thrombospondin-1 and thrombomodulin in human aortic smooth muscle cells.[show abstract] [hide abstract]
ABSTRACT: Plasminogen activator inhibitor-1 (PAI-1), thrombospondin-1 (THBS1) and thrombomodulin (TM) are involved in atherothrombosis. Vitamin D receptor agonists (VDRAs) provide survival/cardiovascular benefits for chronic kidney disease patients. The effects of VDRAs on regulating PAI-1, THBS1 and TM in human aortic smooth muscle cells (SMC) and endothelial cells (EC) were studied. In SMC, paricalcitol and calcitriol downregulated the expression of PAI-1 mRNA and protein in a dose-dependent manner (EC(50) = 0.7 and 4.4 nM, respectively). Both drugs also downregulated THBS1 mRNA and protein (EC(50) = 1.6 and 3.9 nM, respectively). In contrast, paricalcitol and calcitriol upregulated TM mRNA and protein (EC(50) = 28.9 and 25.5 nM, respectively). EC did not express VDR, and VDRAs failed to induce CYP24A1, a VDR target gene. The effect of paricalcitol on THBS1 in SMC was blocked by cycloheximide, while its effect on TM and CYP24A1 was not affected, suggesting that the regulation of THBS1 by VDR may be mediated through intermediate factors, but that TM is likely a direct target of VDR. VDR may play a role in atherothrombosis via regulation of PAI-1, THBS1 and TM.Journal of Vascular Research 02/2007; 44(1):11-8.
Article: Resveratrol, a polyphenolic phytostilbene, inhibits endothelial monocyte chemotactic protein-1 synthesis and secretion.[show abstract] [hide abstract]
ABSTRACT: Resveratrol is a naturally occurring polyphenol phytoestrogen and one of several constituents of red wine thought to be cardioprotective. We investigated the effect of resveratrol on the expression of the atherogenic chemokine, monocyte chemotactic protein-1 (MCP-1). Human umbilical vein endothelial cells were stimulated with interleukin-1beta (IL-1beta) in the absence or presence of resveratrol. MCP-1 levels were determined by ELISA and MCP-1 mRNA was measured. Resveratrol (1-100 microM) dose-dependently inhibited IL-1beta-stimulated MCP-1 secretion, with approximately 45% inhibition at 50 microM resveratrol. This was a Gi-protein- and NO-dependent effect. Resveratrol also significantly inhibited MCP-1 gene expression in a Gi-protein-dependent but NO-independent manner. While resveratrol had no effect on MCP-1 mRNA degradation, it inhibited MCP-1 promoter activity and reduced nuclear factor kappaB and activator protein-1 binding activity induced by IL-1beta. Moreover, while hemoxygenase-1 (HO-1) expression was induced by resveratrol in human umbilical vein endothelial cells, neither treatment with the HO-1 inhibitor tin-protoporphyrin IX nor siRNA-directed knockdown of HO-1 had any effect on the inhibition of MCP-1 mRNA or protein secretion by resveratrol. These data demonstrate an inhibitory effect of resveratrol on MCP-1 synthesis and secretion, mediated via distinct signaling pathways. The inhibition of MCP-1 may represent a novel cardioprotective mechanism of resveratrol.Journal of Vascular Research 02/2007; 44(1):75-84.
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ABSTRACT: Unlike in peripheral vessels, the endothelium-derived hyperpolarizing factor (EDHF)-mediated component to P2Y(2) receptor-mediated dilations is significantly attenuated in the middle cerebral artery (MCA) of female rats compared to male rats. One aspect to the EDHF phenomenon is activation of the intermediate calcium-sensitive potassium (IK(Ca)) channels located on the endothelium. In an attempt to pinpoint the site along the EDHF pathway that is compromised in females, we tested the hypothesis that direct activation of IK(Ca) channels with DCEBIO would elicit attenuated hyperpolarization in the endothelium and smooth muscle of females compared to males. Inhibitors of nitric oxide synthase and cyclooxygenase were present throughout all experiments. Vessel diameter changes were assessed in pressurized and luminally perfused MCAs. Membrane potential changes in the endothelium and smooth muscle were measured using the perforated patch clamp method and sharp electrodes, respectively. The maximum vasodilation to 3 x 10(-4)M DCEBIO was significantly reduced in females (37 +/- 9%) compared to intact males (70 +/- 4%). Endothelial cell hyperpolarization to DCEBIO was similar in both males and females. Smooth muscle cell hyperpolarization was attenuated in females (2 +/- 1 mV) compared to males (15 +/- 3 mV). Taken together, our data suggest that the transfer of hyperpolarization from the endothelium to the smooth muscle is impeded in the female rat MCA.Journal of Vascular Research 02/2007; 44(3):169-74.
Article: Magnetic resonance imaging of ruptured plaques in the rabbit with ultrasmall superparamagnetic particles of iron oxide.[show abstract] [hide abstract]
ABSTRACT: Magnetic resonance imaging (MRI) enhanced with ultrasmall superparamagnetic particles of iron oxide (USPIO) has previously been evaluated in hyperlipidemic rabbits. The aim of this study was therefore to compare USPIO in ruptured and non-ruptured arteries in an atherosclerotic rabbit model. Atherosclerotic-like lesions were induced by the combination of endothelial abrasion and high-cholesterol diet in iliac rabbit arteries (n = 16). Rupture of atherosclerotic lesions was realized by oversized balloon angioplasty in one iliac artery, whereas the contralateral artery was used as control. USPIO (ferumoxtran-10: 1 mmol Fe/kg) was administered immediately (n = 10) or 28 days (n = 6) after injury. MRI and histological analysis were performed 7 and 35 days after injury and in control arteries. In vivo MRI analysis showed extended susceptibility artifact with transluminal signal loss in all ruptured arteries 7 days after injury. In contrast, hyposignal was reduced 35 days following injury (i.e. after healing), and absent in non-ruptured arteries. Similarly, histological analysis of iron uptake was significantly increased 7 days after injury compared to healed-ruptured and control arteries. Accumulation ofUSPIO is significantly increased in ruptured as compared to non-ruptured arteries in the atherosclerotic rabbit model.Journal of Vascular Research 02/2007; 44(2):119-28.
Article: Basement membrane remodeling in skeletal muscles of patients with limb ischemia involves regulation of matrix metalloproteinases and tissue inhibitor of matrix metalloproteinases.[show abstract] [hide abstract]
ABSTRACT: Because the pericapillary basement membrane in skeletal muscles of patients with chronic critical limb ischemia (CLI) is thickened, we determined the expression patterns of genes involved in collagen metabolism, using samples from 9 CLI patients, 4 patients with acute limb ischemia and 4 healthy controls. Gene array analysis, quantitative RT-PCR and semiquantitative grading of immunohistochemical reactivity were performed to determine mRNA/cDNA and protein concentrations. In CLI patients compared to controls, cDNA levels of matrix metalloproteinase (MMP)-9 and MMP-19 were higher, collagen type IV chains A1 and A2, tissue inhibitor of matrix metalloproteinase (TIMP)-1 and TIMP-2 were similar and MMP-2 were lower. On the protein level, MMP-2, MMP-9, MMP-19 and TIMP-1 were more abundantly expressed. In skeletal muscles from patients with acute limb ischemia, cDNA and protein levels of MMP-9, MMP-19, collagen type IV chains, TIMP-1 and TIMP-2 were high. MMP-2 was elevated at the protein but decreased on the cDNA level. Expression of basement membrane components in skeletal muscles of CLI and acute limb ischemia patients is altered, possibly contributing to the pathogenesis of peripheral arterial disease.Journal of Vascular Research 02/2007; 44(3):202-13.
Article: Preferential myosin heavy chain isoform B Expression may contribute to the faster velocity of contraction in veins versus arteries.[show abstract] [hide abstract]
ABSTRACT: Smooth muscle myosin heavy chains occur in 2 isoforms, SMA (slow) and SMB (fast). We hypothesized that the SMB isoform is predominant in the faster-contracting rat vena cava compared to thoracic aorta. We compared the time to half maximal contraction in response to a maximal concentration of endothelin-1 (ET-1; 100 nM), potassium chloride (KCl; 100 mM) and norepinephrine (NE; 10 microM). The time to half maximal contraction was shorter in the vena cava compared to aorta (aorta: ET-1 = 235.8 +/- 13.8 s, KCl = 140.0 +/- 33.3 s, NE = 19.8 +/- 2.7 s; vena cava: ET-1 = 121.8 +/- 15.6 s, KCl = 49.5 +/- 6.7 s, NE = 9.0 +/- 3.3 s). Reverse-transcription polymerase chain reaction supported the greater expression of SMB in the vena cava compared to aorta. SMB was expressed to a greater extent than SMA in the vessel wall of the vena cava. Western analysis determined that expression of SMB, relative to total smooth muscle myosin heavy chains, was 12.5 +/- 4.9-fold higher in the vena cava compared to aorta, while SMA was 4.9 +/- 1.2-fold higher in the aorta than vena cava. Thus, the SMB isoform is the predominant form expressed in rat veins, providing one possible mechanism for the faster response of veins to vasoconstrictors.Journal of Vascular Research 02/2007; 44(4):264-72.
Article: Interferon-beta is a potent inducer of interferon regulatory factor-1/2-dependent IP-10/CXCL10 expression in primary human endothelial cells.[show abstract] [hide abstract]
ABSTRACT: Most virus-infected cells release interferon-beta (IFN-beta) as a powerful inducer of antiviral defense. Endothelial cells tightly regulate local immune cell recruitment by expression of adhesion molecules and chemokines. Here, we studied the transcriptional regulation of IFN-beta-induced chemokine expression in primary human endothelial cells. IFN-beta moderately increased monocyte chemoattractant protein-1/CCL2 and potently raised IFN-gamma-inducible protein-10/CXCL10 mRNA steady-state levels and protein release, while no effect was detected on various other chemokines. As shown by transient transfections, induction of CXCL10 expression depends on an IFN-stimulated response element (ISRE) within the CXCL10 promoter. A double point mutation of the putative IFN regulatory factor (IRF)-1/2 binding site within this ISRE motif abolished IFN-beta-induced promoter activity. In electrophoretic mobility shift assays, this ISRE motif showed a basal IRF-2 and an IFN-beta-inducible IRF-1 and augmented IRF-2 binding. Furthermore, stimulation with IFN-beta induced a rapid nuclear translocation of signal transducer and activator of transcription 1 (STAT1) and STAT2 and their transient binding to a gamma-activated site within the CCL2 promoter. The kinetics of transient STAT1 binding to this gamma-activated site element correlated with the amount of Y701-phosphorylated nuclear STAT1, while S727-phosphorylated nuclear STAT1 remained stable over 24 h after stimulation. Therefore, IFN-beta potently induces endothelial chemokine expression at the transcriptional level.Journal of Vascular Research 02/2007; 44(1):51-60.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.
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