163 results on '"Aortic endothelium"'
Search Results
2. Uremic serum induces prothrombotic changes in venous endothelial cells and inflammatory changes in aortic endothelial cells.
- Author
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Sosińska-Zawierucha, Patrycja and Bręborowicz, Andrzej
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ENDOTHELIAL cells , *TISSUE plasminogen activator , *KIDNEY failure , *VASCULAR endothelial growth factors , *CELL adhesion molecules , *VON Willebrand disease , *AORTA , *VON Willebrand factor - Abstract
Uremia induces various pathologic changes in the endothelium. However, there is limited information about the differences of these effects in endothelial cells originating from different parts of the vascular tree. The effect of uremic serum obtained from patients with end stage renal failure on the gene expression and secretory activity of venous endothelial cells (VEC) and aortic endothelial cells (AEC) was studied in in vitro culture. In VEC, the expression of genes regulating the synthesis of von Willebrand factor (vWF) was increased by 254% (p<.005), vascular endothelial growth factor (VEGF) synthesis by 150% (p<.001), tissue plasminogen activator (t-PA) synthesis by 62% (p<.005), platelet endothelial cell adhesion molecule by 89% (p<.005), and the expression of gene regulating interleukin-6 (IL-6) synthesis was reduced. In AEC, the expression of the gene regulating synthesis of IL-6 was increased by 174% (p<.001), and the expression of the other genes was reduced. The secretion of IL-6 was reduced in VEC by 38% (p<.01) and increased in AEC by 55% (p<.005). In VEC, increased synthesis of VEGF 64% (p<.001) vWF (+34%, p<.01), and t-PA (+53%, p<.002) was observed, and in AEC it was reduced. VEC and AEC respond in different ways after exposure to uremic serum. VEC acquires the prothrombotic phenotype, whereas in AEC the inflammatory phenotype appears. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
3. Protein-bounded uremic toxin p-cresylsulfate induces vascular permeability alternations.
- Author
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Tang, Wei-Hua, Wang, Chao-Ping, Yu, Teng-Hung, Tai, Pei-Yang, Liang, Shih-Shin, Hung, Wei-Chin, Wu, Cheng-Ching, Huang, Sung-Hao, Lee, Yau-Jiunn, and Chen, Shih-Chieh
- Subjects
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EVANS blue , *KIDNEY diseases , *IMMUNOGLOBULIN G , *ENDOTHELIUM diseases , *INTRAPERITONEAL injections - Abstract
The goal of the present studies is to investigate that the impact of p-cresylsulfate (PCS) on the endothelial barrier integrity via in situ exposure and systemic exposure. Vascular permeability changes induced by local injection of PCS were evaluated by the techniques of both Evans blue (EB) and India ink tracer. Rats were intravenously injected with EB or India ink followed by intradermal injections of various doses of PCS (0, 0.4, 2, 10 and 50 µmol/site) on rat back skins. At different time points, skin EB was extracted and quantified. The administration of India ink was used to demonstrate leaky microvessels. Skin PCS levels were also determined by liquid chromatography-mass spectrometry. We also investigated whether the increased endothelial leakage occurred in the aortic endothelium in rats treated with 5/6 nephrectomy and intraperitoneal injection of PCS 50 mg/kg/day for 4 weeks. The aortic endothelial integrity was evaluated by increased immunoglobulin G (IgG) leakage. High doses of PCS, but not lower doses, significantly induced vascular leakage as compared to saline injection and EB leakage exhibited in time-dependent manner. A time-correlated increase in leaky microvessels was detected in the tissues examined. The injected PCS declined with time and displayed an inverse relationship with vascular leakage. Chronic kidney disease (CKD) rats administered with PCS, compared to control rats, had significantly higher serum levels of PCS and apparent IgG deposition in the aortic intima. Increased endothelial leakage induced by PCS in skin microvessels and the aorta of CKD rats suggests that the PCS-induced endothelial barrier dysfunction. [ABSTRACT FROM AUTHOR]
- Published
- 2018
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4. Age-Related Changes in the Expression of ICAM-1 in the Aorta of Wistar Albino Rats.
- Author
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Ketani, Sennur, Karakoç, Zelal, Ketani, M. Aydın, and Kilinç, Mehmet
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BLOOD circulation , *BLOOD flow , *ENDOTHELIAL cells , *LEUCOCYTES , *PATHOGENIC microorganisms - Abstract
ICAM-1 which is expressed by endothelial cells and leukocytes are observed as first markers in diseases such as transplant rejection, diabetes and atherosclerosis and in infections caused by various pathogens. In the present study, it is aimed to reveal the age-related changes in the expression of ICAM-1 on rats. Therefore, a total of 30 albino rats were taken at the age of 6, 18 and 24 months without gender discrimination. Rats were fed with standard pellet feed during the study. Afterwards, rats were sacrificed and tissue samples were collected from their rats, and the samples were evaluated under the light microscope by staining with immnunohistochemical method. It was determined that the expression of both aortic endothelial cells and endothelial cells in the media layer had been significantly increased based on the age. [ABSTRACT FROM AUTHOR]
- Published
- 2016
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5. Development and Characterization of SV40 Large T Immortalized Endothelial Cells of the Rat Blood-Brain and Blood-Retinal Barriers
- Author
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Adamson, P., Pryce, G., Calder, V., Greenwood, J., Couraud, Pierre-Olivier, editor, and Scherman, Daniel, editor
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- 1996
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6. The Effects of Nicotine on Aortic Endothelial Cell Turnover and Ultrastructure
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Zimmerman, Matthew, McGeachie, John K., and Diana, John N., editor
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- 1990
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7. Endothelial HuR deletion reduces the expression of proatherogenic molecules and attenuates atherosclerosis
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Ji Yuan, Shuiting Zhai, and Xiaoyang Fu
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0301 basic medicine ,Endothelium ,Immunology ,Inflammation ,030204 cardiovascular system & hematology ,Chronic inflammatory disease ,ELAV-Like Protein 1 ,Pathogenesis ,Mice ,03 medical and health sciences ,Apolipoproteins E ,0302 clinical medicine ,Cell Movement ,Cell Adhesion ,Leukocytes ,medicine ,Animals ,Humans ,Immunology and Allergy ,Arterial wall ,Aorta ,Cells, Cultured ,Mice, Knockout ,Pharmacology ,Chemistry ,Lipid metabolism ,Atherosclerosis ,Cell biology ,Mice, Inbred C57BL ,030104 developmental biology ,medicine.anatomical_structure ,cardiovascular system ,Aortic endothelium ,Endothelium, Vascular ,medicine.symptom - Abstract
Atherosclerosis is a chronic inflammatory disease of arterial wall, and the proatherogenic molecules derived from endothelium and leukocyte recruitment are major contributors to its pathogenesis. The RNA-binding protein HuR plays several physiological roles in endothelial cells, but its relevance to atherosclerosis is not yet determined. Here, by utilizing the ApoE-/- mice depleted of endothelia HuR (ApoE-/-; HuRfl/fl; Cdh5-Cre), we observed that these mice exhibited attenuated atherosclerosis compared with wild-type littermates (ApoE-/-; HuRfl/fl). Mechanistically, this phenomenon may not be associated with systemic effects on lipid metabolism, however, we found that the expression levels of proatherogenic molecules, degree of local inflammation and extent of leukocyte recruitment to aortic endothelium were all decreased when endothelia HuR was absent. Collectively, our study uncovers the role of endothelia HuR deletion in attenuating atherosclerosis, and suggests that this effect is at least in part attributed to the decreased expression of proatherogenic molecules and suppressed local inflammation. Hence, our study might offer a potential strategy for atherosclerosis treatment via manipulating endothelia HuR.
- Published
- 2018
8. Hapin1b, a central organizer of the ECM, modulates kit signaling to control developmental hematopoiesis in zebrafish
- Author
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Mahony, Christopher B., Cacialli, Pietro, Pasche, Corentin, Monteiro, Rui, Savvides, Savvas, and Bertrand, Julien Y.
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PERINEURONAL NETS ,BINDING ,Medicine and Health Sciences ,EXTRACELLULAR-MATRIX ,PROGENITOR ,Biology and Life Sciences ,AORTIC ENDOTHELIUM ,STEM-CELL EMERGENCE ,GENERATING PRECEREBELLAR NUCLEUS ,HEMOGENIC ENDOTHELIUM ,TRANSITION ,EXPRESSION PATTERN - Abstract
During early vertebrate development, hematopoietic stem and progenitor cells (HSPCs) are produced in hemogenic endothelium located in the dorsal aorta, before they migrate to a transient niche where they expand to the fetal liver and the caudal hematopoietic tissue, in mammals and zebrafish, respectively. In zebrafish, previous studies have shown that the extracellular matrix (ECM) around the aorta must be degraded to enable HSPCs to leave the aortic floor and reach blood circulation. However, the role of the ECM components in HSPC specification has never been addressed. In this study, haplalb, a key component of the ECM, was specifically expressed in hematopoietic sites in the zebrafish embryo. Gain- and loss-of-function experiments all resulted in the absence of HSPCs in the early embryo, showing that hapinlb is necessary, at the correct level, to specify HSPCs in the hemogenic endothelium. Furthermore, the expression of hapinlb was necessary to maintain the integrity of the ECM through its link domain. By combining functional analyses and computer modeling, we showed that kitigb interacts with the ECM to specify HSPCs. The findings show that the ECM is an integral component of the microenvironment and mediates the cytokine signaling that is necessary for HSPC specification.
- Published
- 2021
9. Aerobic Exercise Prevents Insulin Resistance Through the Regulation of miR-492/Resistin Axis in Aortic Endothelium
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Suixin Liu, Ying Cai, Kang-Ling Xie, and Fan Zheng
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Blood Glucose ,Male ,0301 basic medicine ,medicine.medical_specialty ,Mice, Knockout, ApoE ,Aortic Diseases ,Regulator ,Pharmaceutical Science ,030204 cardiovascular system & hematology ,03 medical and health sciences ,0302 clinical medicine ,Insulin resistance ,Downregulation and upregulation ,Internal medicine ,Genetics ,medicine ,Animals ,Aerobic exercise ,Resistin ,Aorta ,Swimming ,Genetics (clinical) ,business.industry ,nutritional and metabolic diseases ,Lipid metabolism ,Atherosclerosis ,medicine.disease ,Lipids ,Plaque, Atherosclerotic ,Exercise Therapy ,Mice, Inbred C57BL ,Disease Models, Animal ,MicroRNAs ,030104 developmental biology ,Endocrinology ,Gene Expression Regulation ,Aortic endothelium ,Molecular Medicine ,Insulin Resistance ,Cardiology and Cardiovascular Medicine ,business ,Biomarkers ,hormones, hormone substitutes, and hormone antagonists ,Signal Transduction - Abstract
Previously, we found that miR-492 delayed the progression of atherosclerosis (AS) by acting as an up-stream regulator of resistin. Therefore, we hypothesized that the anti-atherogenic effects of exercise are related to miR-492-mediated downregulation of resistin and repair of endothelial injury. In this study, we investigated the effects of the miR-492/resistin axis on improving endothelial injury in ApoE-/- mice (ApoE-deficient/knockout in C57BL/6 mice) through swimming exercises. Our results showed that the severity of AS and insulin resistance (IR) in these mice were significantly reduced by swimming exercises. In addition, miR-492 expression in the aortic endothelium of ApoE-/- mice was decreased, in addition to increased levels of resistin. Interestingly, swimming exercises increased miR-492 expression while decreasing that of resistin. Taken together, swimming exercises delayed the progression of AS, possibly by upregulating miR-492 and downregulating resistin in aortic endothelium. Therefore, exercises modulated glucose and lipid metabolism, alleviated endothelial IR, and repaired endothelial injury.
- Published
- 2018
10. Obesity suppresses circulating level and function of endothelial progenitor cells and heart function.
- Author
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Tzu-Hsien Tsai, Han-Tan Chai, Cheuk-Kwan Sun, Chia-Hung Yen, Steve Leu, Yung-Lung Chen, Sheng-Ying Chung, Sheung-Fat Ko, Hsueh-Wen Chang, Chiung-Jen Wu, and Hon-Kan Yip
- Subjects
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OBESITY , *PROGENITOR cells , *HEART function tests , *ISCHEMIA , *NEOVASCULARIZATION - Abstract
Background and aim: This study tested the hypothesis that obesity suppresses circulating number as well as the function of endothelial progenitor cells (EPCs) and left ventricular ejection fraction (LVEF). Methods: High fat diet (45 Kcal% fat) was given to 8-week-old C57BL/6 J mice (n = 8) for 20 weeks to induce obesity (group 1). Another age-matched group (n = 8) were fed with control diet for 20 weeks as controls (group 2). The animals were sacrificed at the end of 20 weeks after obesity induction. Results: By the end of study period, the heart weight, body weight, abdominal fat weight, serum levels of total cholesterol and fasting blood sugar were remarkably higher in group 1 than in group 2 (all p<0.01). The circulating level of EPCs (C-kit/CD31, Sca-1/KDR, CXCR4/CD34) was significantly lower in group 1 than in group 2 (p<0.03) at 18 h after critical limb ischemia induction. The angiogenesis and migratory ability of bone marrow-derived EPCs was remarkably impaired in group 1 compared to that in group 2 (all p<0.01). The repair ability of aortic endothelium damage by lipopolysaccharide was notably attenuated in group 1 compared with that in group 2 (p<0.01). Collagen deposition (Sirius red staining) and fibrotic area (Masson's Trichrome staining) in LV myocardium were notably increased in group 1 compared with group 2 (p<0.001). LVEF was notably lower, whereas LV end-diastolic and end-systolic dimensions were remarkably higher in group 1 than in group 2 (all p<0.001). Conclusions: Obesity diminished circulating EPC level, impaired the recovery of damaged endothelium, suppressed EPC angiogenesis ability and LVEF, and increased LV remodeling. [ABSTRACT FROM AUTHOR]
- Published
- 2012
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11. A mechanism by which dietary trans fats cause atherosclerosis
- Author
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Chen, Chun-Lin, Tetri, Laura H., Neuschwander-Tetri, Brent A., Huang, Shuan Shian, and Huang, Jung San
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TRANS fatty acids , *ATHEROSCLEROSIS , *TRANSFORMING growth factors , *CHOLESTEROL , *CELL membranes , *HYPERCHOLESTEREMIA , *ENDOTHELIUM - Abstract
Abstract: Dietary trans fats (TFs) have been causally linked to atherosclerosis, but the mechanism by which they cause the disease remains elusive. Suppressed transforming growth factor (TGF)-β responsiveness in aortic endothelium has been shown to play an important role in the pathogenesis of atherosclerosis in animals with hypercholesterolemia. We investigated the effects of a high TF diet on TGF-β responsiveness in aortic endothelium and integration of cholesterol in tissues. Here, we show that normal mice fed a high TF diet for 24 weeks exhibit atherosclerotic lesions and suppressed TGF-β responsiveness in aortic endothelium. The suppressed TGF-β responsiveness is evidenced by markedly reduced expression of TGF-β type I and II receptors and profoundly decreased levels of phosphorylated Smad2, an important TGF-β response indicator, in aortic endothelium. These mice exhibit greatly increased integration of cholesterol into tissue plasma membranes. These results suggest that dietary TFs cause atherosclerosis, at least in part, by suppressing TGF-β responsiveness. This effect is presumably mediated by the increased deposition of cholesterol into cellular plasma membranes in vascular tissue, as in hypercholesterolemia. [Copyright &y& Elsevier]
- Published
- 2011
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12. L'endothélium aortique chez l'embryon : genèse et rôle dans l'hématopoïèse.
- Author
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Jaffredo, Thierry
- Published
- 2009
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13. Hepatic Sinusoidal Endothelium Upregulates IL-1α, IFN-γ, and iNOS in Response to Discordant Xenogeneic Islets in an in Vitro Model of Xenoislet Transplantation
- Author
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Tan, Michael, Di Carlo, Antonio, Liu, Shu Qing, Tector, A. Joseph, Tchervenkov, Jean I., and Metrakos, Peter
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ENDOTHELIUM , *CYTOKINES - Abstract
Background. Data indicate that early islet graft failure is due to nonspecific inflammatory mechanisms that occur prior to T-cell-mediated rejection. The role of the host hepatic endothelium in mediating this immediate islet injury has not been elucidated. The endothelial cell may be important in this process because it is essentially the first cellular barrier encountered by intraportally introduced islets. We have characterized the initial response of hepatic endothelium to xenogeneic islets by measuring the expression of Il-1α, TNF-α, IFN-γ, and iNOS in an in vitro dog-to-pig model of xenoislet transplantation.Materials and methods. Dog islets (500 islet equivalents) were cocultured with either porcine hepatic endothelium or porcine aortic endothelium over a 24-h period in serum-free medium. RNA was extracted at eight time points (0, 1, 2, 4, 6, 8, 12, and 24 h). Reverse-transcriptase polymerase chain reaction was performed on each sample. Polymerase chain reaction was done on the cDNA in order to visualize Il-1α, TNF-α, IFN-γ, and iNOS expression. Bands were semiquantitated by comparison to an external standard (GAPDH) using band densitometry.Results. Hepatic endothelium had early (1 h) expression of IL-1α, IFN-γ, and iNOS. IL-1α peaked at 2 h, IFN-γ at 12 h, and iNOS at 1 and 12 h. Aortic endothelium expressed low levels of IL-1α and TNF-α, but not IFN-γ or iNOS.Conclusions. We have demonstrated that xenogeneic islets are able to activate host endothelial cells without serum or immune cells. The observed endothelial response corresponds with known islet toxic substances. Furthermore, the response differs between hepatic and aortic endothelial cells, suggesting that these differences may be important in choosing suitable implantation sites for islets. Our findings suggest that host endothelium may play an important part in early injury of islet xenotransplants. [Copyright &y& Elsevier]
- Published
- 2002
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14. Sitagliptin inhibits endothelin-1 expression in the aortic endothelium of rats with streptozotocin-induced diabetes by suppressing the nuclear factor-κB/IκBα system through the activation of AMP-activated protein kinase
- Author
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Qing Zhou, Hai-qin Tang, Qiu Zhang, Huaqing Zhu, Yuan Wang, Song-tao Tang, Chang-jiang Wang, Wei Wei, and Huan-Huan Su
- Subjects
Male ,0301 basic medicine ,Arteriosclerosis ,AMP-Activated Protein Kinases ,030204 cardiovascular system & hematology ,Rats, Sprague-Dawley ,0302 clinical medicine ,Glucagon-Like Peptide 1 ,Endothelial dysfunction ,Aorta ,Endothelin-1 ,diabetes ,NF-kappa B ,Articles ,General Medicine ,I-kappa B Kinase ,medicine.anatomical_structure ,Sitagliptin ,Signal Transduction ,medicine.drug ,medicine.medical_specialty ,Endothelium ,Diet, High-Fat ,Nitric Oxide ,Streptozocin ,sitagliptin ,Diabetes Mellitus, Experimental ,Sitagliptin Phosphate ,aortic endothelium ,03 medical and health sciences ,Internal medicine ,Genetics ,medicine ,Animals ,Hypoglycemic Agents ,Dipeptidyl-Peptidase IV Inhibitors ,Dose-Response Relationship, Drug ,business.industry ,AMPK ,Streptozotocin ,medicine.disease ,Endothelin 1 ,Rats ,IκBα ,030104 developmental biology ,Endocrinology ,Gene Expression Regulation ,Endothelium, Vascular ,business - Abstract
Emerging evidence suggests that dipeptidyl peptidase-4 (DPP-4) inhibitors, including sitagliptin, exert favourable effects on the vascular endothelium. DPP-4 inhibitors suppress the degradation of glucagon-like peptide-1 (GLP-1), which has been reported to enhance nitric oxide (NO) production. However, the effects of DPP-4 inhibitors on endothelin-1 (ET-1) expression in the aorta, as well as the underlying mechanisms responsible for these effects, have yet to be investigated in animal models of diabetes mellitus (DM). In the present study, the rats were randomly divided into the following four groups: i) control; ii) DM; iii) DM + low-dose sitagliptin (10 mg/kg); and iv) DM + high-dose sitagliptin (30 mg/kg). Apart from the control group, all the rats received a high-fat diet for 8 weeks prior to the induction of diabetes with an intraperitoneal injection of streptozotocin. The treatments were then administered for 12 weeks. The serum levels of ET-1, NO, GLP-1 and insulin were measured as well as endothelial function. The expression of ET-1, AMP-activated protein kinase (AMPK) and nuclear factor (NF)-κB/IκBα were determined. After 12 weeks of treatment, the diabetic rats receiving sitagliptin showed significantly elevated serum levels of GLP-1 and NO, and reduced levels of ET-1. Moreover, sitagliptin significantly attenuated endothelial dysfunction as well as the remodeling of the aortic wall. Notably, sitagliptin inhibited ET-1 expression at the transcriptional and translational level in the aorta, which may have been mediated by the suppression of the NF-κB/IκBα system induced by AMPK activation. The majority of the above-mentioned effects were dose dependent. Taken together, the findings of the present study indicate that sitagliptin inhibits ET-1 expression in the aortic endothelium by suppressing the NF-κB/IκBα system through the activation of the AMPK pathway in diabetic rats. These findings further demonstrate some of the vasoprotective properties of DPP-4 inhibitors in vivo.
- Published
- 2016
15. Obesity suppresses circulating level and function of endothelial progenitor cells and heart function
- Author
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Tsai Tzu-Hsien, Chai Han-Tan, Sun Cheuk-Kwan, Yen Chia-Hung, Leu Steve, Chen Yung-Lung, Chung Sheng-Ying, Ko Sheung-Fat, Chang Hsueh-Wen, Wu Chiung-Jen, and Yip Hon-Kan
- Subjects
Obesity ,Aortic endothelium ,Endothelial progenitor cells ,Angiogenesis ,Left ventricular remodeling ,Medicine - Abstract
Abstract Background and aim This study tested the hypothesis that obesity suppresses circulating number as well as the function of endothelial progenitor cells (EPCs) and left ventricular ejection fraction (LVEF). Methods High fat diet (45 Kcal% fat) was given to 8-week-old C57BL/6 J mice (n = 8) for 20 weeks to induce obesity (group 1). Another age-matched group (n = 8) were fed with control diet for 20 weeks as controls (group 2). The animals were sacrificed at the end of 20 weeks after obesity induction. Results By the end of study period, the heart weight, body weight, abdominal fat weight, serum levels of total cholesterol and fasting blood sugar were remarkably higher in group 1 than in group 2 (all p Conclusions Obesity diminished circulating EPC level, impaired the recovery of damaged endothelium, suppressed EPC angiogenesis ability and LVEF, and increased LV remodeling.
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- 2012
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16. Aortic endothelium of alloxan diabetic rabbits: A quantitative study using scanning electron microscopy.
- Author
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Dolgov, V., Zaikina, O., Bondarenko, M., and Repin, V.
- Abstract
Scanning electron microscope studies of the aorta and other major arteries have been performed in alloxan-induced diabetic rabbits. After 5 weeks, a variety of structural abnormalities of the endothelial lining were detected including a significant increase in the number of argyrophilic cells and an increased number of craters or openings in the endothelial junctional region. Evidence of more extensive micro-damage was present after 5 months duration of diabetes. These zones with structural changes in the endothelial lining of major vessels seem to be areas of high predilection to atherosclerosis in diabetes. [ABSTRACT FROM AUTHOR]
- Published
- 1982
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17. Ultrastructural localization of NADPH-diaphorase and colocalization of nitric oxide synthase in endothelial cells of the rabbit aorta.
- Author
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Loesch, Andrzej, Belai, Abebech, and Burnstock, Geoffrey
- Abstract
This is the first report on the ultrastructural pattern of distribution of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) in endothelial cells, using the rabbit aorta, and its colocalization with the neuronal isoform (type I) of nitric oxide synthase. About 30% of the endothelial cells showed a positive reaction for NADPH-d compared to about 6% for nitric oxide synthase immunoreactivity. Simultaneous double histochemical-immunocytochemical labelling procedures indicate that all of the cells displaying nitric oxide synthase-positive reactivity also contained NADPH-d; the remainder of NADPH-d-positive endothelial cells were negative for this isoform of nitric oxide synthase. Nitric oxide synthase-immunogold labelling was mostly associated with free ribosomes, while NADPH-d activity was distributed largely in patches in the cytoplasm and in association with the cell membrane. [ABSTRACT FROM AUTHOR]
- Published
- 1993
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18. Cytokinetic studies on the aortic endothelium and limb bud vascularization in avian embryos.
- Author
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Seifert, R., Zhao, B., and Christ, B.
- Abstract
Cytokinetic studies on the aortic endothelium using the BrdU/anti-BrdU-method were carried out on 2.5- to 6-day chick and quail embryos. The mitotic activity of the aortic endothelium is related temporally to the age of the avian embryo and spatially to the embryonic region where the aorta originates. The mitotic activity of the aortic endothelium decreases with increasing age of the embryos. In the limb buds, however, the mitotic rate of the aortic endothelial cells increases independently of the age of the embryo. This increase in the mitotic activity of the aortic endothelium at the appropriate levels coincides with the vascularization of the outgrowing limb buds. We concluded therefore that the aortic endothelium probably supplies endothelial cells for the formation of limb vessels at this stage. Thus our results suggest that angiogenesis (sprouting of capillaries from pre-existing vessels) takes place during limb vascularization in avian embryos. On the other hand, immunohistochemical studies with QH-1 or MB-1 antibody show, beside a capillary network in the central core of the wing bud, individual immunolabelled cells of mesenchymal character within the primarily avascular subectodermal region from the onset of vascularization onwards. We suggest that these cells have partly to be regarded as endothelial precursor cells, which have differentiated in situ from the local limb mesenchyme, and which will contribute to the developing vascular plexus. This means that not only angiogenesis, but also vasculogenesis (in situ from mesenchymal precursors differentiated endothelial cells) appears to be involved in limb vessel formation. [ABSTRACT FROM AUTHOR]
- Published
- 1992
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19. Development and Multiparametric Evaluation of Experimental Atherosclerosis in Rabbits
- Author
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Max L. Senders, Zahi A. Fayad, Carlos Pérez-Medina, Francois Fay, Claudia Calcagno, Raphael Soler, Mark E. Lobatto, Olivier Lairez, Willem J. M. Mulder, ACS - Atherosclerosis & ischemic syndromes, Graduate School, 01 Internal and external specialisms, Radiology and Nuclear Medicine, and Medical Biochemistry
- Subjects
0301 basic medicine ,Experimental atherosclerosis ,medicine.medical_specialty ,Pathology ,biology ,business.industry ,Rabbit (nuclear engineering) ,030204 cardiovascular system & hematology ,biology.organism_classification ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,New Zealand white rabbit ,In vivo ,medicine ,Aortic endothelium ,Histopathology ,business ,Large size - Abstract
Several animal models have been developed to study atherosclerosis. Here we present a rabbit atherosclerosis model generated by surgical denudation of the aortic endothelium in combination with a high-fat and cholesterol-enriched diet. This model is characterized by the formation of vascular lesions that exhibit several hallmarks of human atherosclerosis. Due to the rabbit’s relative large size, as compared to rodents, this model is suited for the imaging-guided evaluation of novel therapeutic strategies using clinical scanners. In this chapter, we present an extensive outline of the procedures to induce aortic atherosclerotic lesions in rabbits as well as methods to evaluate the disease, including noninvasive in vivo multiparametric imaging and histopathology.
- Published
- 2018
20. Macrophage-pathogen interactions in infectious diseases: new therapeutic insights from the zebrafish host model
- Author
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Annemarie H. Meijer, Vincenzo Torraca, Herman P. Spaink, and Samrah Masud
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Staphylococcus ,AORTIC ENDOTHELIUM ,Medicine (miscellaneous) ,lcsh:Medicine ,Review ,Animals, Genetically Modified ,Immunology and Microbiology (miscellaneous) ,Salmonella ,Pathology ,MEDIATES RESISTANCE ,Pathogen ,Zebrafish ,IN-VIVO ,Organism ,Candida ,STAPHYLOCOCCUS-AUREUS INFECTIONS ,Innate immunity ,Infectious disease ,11 Medical And Health Sciences ,INNATE IMMUNE-RESPONSE ,3. Good health ,Cell biology ,Leukocyte biology ,T cell subset ,Host-Pathogen Interactions ,MYCOBACTERIUM-TUBERCULOSIS ,Life Sciences & Biomedicine ,lcsh:RB1-214 ,Burkholderia ,Neuroscience (miscellaneous) ,Host model ,Biology ,Communicable Diseases ,BURKHOLDERIA-CEPACIA COMPLEX ,General Biochemistry, Genetics and Molecular Biology ,Host-directed therapy ,Mycobacterium ,lcsh:Pathology ,Animals ,Science & Technology ,Innate immune system ,Intracellular parasite ,Macrophages ,lcsh:R ,SALMONELLA-TYPHIMURIUM ,Cell Biology ,06 Biological Sciences ,biology.organism_classification ,Disease Models, Animal ,Infectious disease (medical specialty) ,INDUCIBLE NITRIC-OXIDE ,TUBERCULOUS GRANULOMA ,Shigella ,Developmental Biology - Abstract
Studying macrophage biology in the context of a whole living organism provides unique possibilities to understand the contribution of this extremely dynamic cell subset in the reaction to infections, and has revealed the relevance of cellular and molecular processes that are fundamental to the cell-mediated innate immune response. In particular, various recently established zebrafish infectious disease models are contributing substantially to our understanding of the mechanisms by which different pathogens interact with macrophages and evade host innate immunity. Transgenic zebrafish lines with fluorescently labeled macrophages and other leukocyte populations enable non-invasive imaging at the optically transparent early life stages. Furthermore, there is a continuously expanding availability of vital reporters for subcellular compartments and for probing activation of immune defense mechanisms. These are powerful tools to visualize the activity of phagocytic cells in real time and shed light on the intriguing paradoxical roles of these cells in both limiting infection and supporting the dissemination of intracellular pathogens. This Review will discuss how several bacterial and fungal infection models in zebrafish embryos have led to new insights into the dynamic molecular and cellular mechanisms at play when pathogens encounter host macrophages. We also describe how these insights are inspiring novel therapeutic strategies for infectious disease treatment.
- Published
- 2014
21. Vasomotor Activity of the Aorta during Chronic Smoking Modeling
- Author
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I. G. Agafonova, Vera Nevzorova, Elena Gonchar, and N. V. Zakharchuk
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medicine.medical_specialty ,Vasodilation ,Statistics, Nonparametric ,General Biochemistry, Genetics and Molecular Biology ,Tobacco smoke ,Pulmonary Disease, Chronic Obstructive ,medicine.artery ,Internal medicine ,medicine ,Animals ,Pathological ,Aorta ,integumentary system ,Inhalation ,Vasomotor ,business.industry ,Smoking ,Endothelial Cells ,General Medicine ,Magnetic Resonance Imaging ,Rats ,Vasomotor System ,Disease Models, Animal ,Vasoconstriction ,cardiovascular system ,Aortic endothelium ,Cardiology ,medicine.symptom ,business ,circulatory and respiratory physiology - Abstract
We studied vasomotor responses of aortic endothelium in a rat model of chronic smoking. It was found that long-term exposure to tobacco smoke (inhalation) impaired vasomotor function of the aortic endothelium leading to insufficient vasodilator activity and enhanced vasoconstriction. After the cessation of inhalations, vasomotor disturbances were not only preserved, but also exacerbated because of increased pathological endothelium-independent vasoconstriction.
- Published
- 2013
22. Adenosine Uptake and Adenine Nucleotide Metabolism by Vascular Endothelium
- Author
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Pearson, Jeremy D., Hellewell, Paul G., Gordon, John L., Berne, Robert M., editor, Rall, Theodore W., editor, and Rubio, Rafael, editor
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- 1983
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23. The Role of Arterial Endothelial Cell Mitosis in Macromolecular Permeability
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Chien, Shu, Lin, Shing-Jong, Weinbaum, Sheldon, Lee, Mary M. L., Jan, Kung-Ming, and Chien, Shu, editor
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- 1988
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24. Endothelium and the Vessel Wall
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Pittilo, R. Michael, Tinker, Jack, editor, Pittilo, R. Michael, editor, and Machin, Samuel J., editor
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- 1988
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25. Injury at the Vascular Surface
- Author
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Schwartz, S. M., Reidy, M. A., Hansson, G. K., Schettler, Gotthard, editor, Nerem, Robert M., editor, Schmid-Schönbein, Holger, editor, Mörl, Hubert, editor, and Diehm, Curt, editor
- Published
- 1983
- Full Text
- View/download PDF
26. Response of Vascular Endothelium to Unsteady Fluid Shear Stress in Vitro
- Author
-
Dewey, C. F., Jr., Gimbrone, M. A., Jr., Bussolari, S. R., White, G. E., Davies, P. F., Schettler, Gotthard, editor, Nerem, Robert M., editor, Schmid-Schönbein, Holger, editor, Mörl, Hubert, editor, and Diehm, Curt, editor
- Published
- 1983
- Full Text
- View/download PDF
27. Aortic Endothelial Changes During the Development and Reversal of Experimental Hypertension
- Author
-
Chobanian, Aram V., Prescott, Margaret Forney, Haudenschild, Christian C., Gotto, Antonio M., Jr., editor, Smith, Louis C., editor, and Allen, Barbara, editor
- Published
- 1980
- Full Text
- View/download PDF
28. Endothelial Dysfunction and the Pathogenesis of Atherosclerosis
- Author
-
Gimbrone, Michael A., Jr, Gotto, Antonio M., Jr., editor, Smith, Louis C., editor, and Allen, Barbara, editor
- Published
- 1980
- Full Text
- View/download PDF
29. Platelet and Endothelial Alterations in Experimental Arteriosclerosis
- Author
-
Harker, Laurence A., Gotto, Antonio M., Jr., editor, Smith, Louis C., editor, and Allen, Barbara, editor
- Published
- 1980
- Full Text
- View/download PDF
30. Ultrastructure of the Normal Arterial Endothelium and Intima
- Author
-
Schwartz, Colin J., Gerrity, Ross G., Sprague, Eugene A., Hagens, M. Robin, Reed, Carol T., Guerrero, Daniel L., Gotto, Antonio M., Jr., editor, Smith, Louis C., editor, and Allen, Barbara, editor
- Published
- 1980
- Full Text
- View/download PDF
31. Lipid Accumulation in the Vessel Wall
- Author
-
Moore, S., Camilleri, Jean-Pierre, editor, Berry, Colin L., editor, Fiessinger, Jean-Noël, editor, and Bariéty, Jean, editor
- Published
- 1989
- Full Text
- View/download PDF
32. Age-Related Changes in the Expression of ICAM-1 in the Aorta of Wistar Albino Rats
- Author
-
Sennur Ketani, Zelal Karakoç, Mehmet Kilinç, M. Aydın Ketani, and Belirlenecek
- Subjects
0301 basic medicine ,03 medical and health sciences ,030104 developmental biology ,Age ,business.industry ,ICAM-1 ,Medicine ,Rat ,Aortic endothelium ,Anatomy ,business - Abstract
ICAM-1 which is expressed by endothelial cells and leukocytes are observed as first markers in diseases such as transplant rejection, diabetes and atherosclerosis and in infections caused by various pathogens. In the present study, it is aimed to reveal the age-related changes in the expression of ICAM-1 on rats. Therefore, a total of 30 albino rats were taken at the age of 6, 18 and 24 months without gender discrimination. Rats were fed with standard pellet feed during the study. Afterwards, rats were sacrificed and tissue samples were collected from their rats, and the samples were evaluated under the light microscope by staining with immnunohistochemical method. It was determined that the expression of both aortic endothelial cells and endothelial cells in the media layer had been significantly increased based on the age.
- Published
- 2016
- Full Text
- View/download PDF
33. Hemodynamic Forces Induce the Release of Nitric Oxide from Aortic Endothelium: Combined Effect of Shear Stress and Pressure
- Author
-
Husain S. Yawer, Sadik R. Panwar, Shakir Ali, Nidhi Priya, and Alok R Rays
- Subjects
chemistry.chemical_compound ,medicine.medical_specialty ,chemistry ,Internal medicine ,Aortic endothelium ,Shear stress ,medicine ,Cardiology ,Ocean Engineering ,Hemodynamic forces ,Nitric oxide - Published
- 2018
34. DESIGN OF A NOVEL STENTED VALVE AND 3D MODELING OF ITS IMPLANTATION IN THE AORTA
- Author
-
Gideon Praveen Kumar and Lazar Mathew
- Subjects
Aortic valve ,Aorta ,medicine.medical_specialty ,Percutaneous aortic valve replacement ,Percutaneous ,business.industry ,medicine.medical_treatment ,Biomedical Engineering ,Biophysics ,Stent ,Bioengineering ,equipment and supplies ,Surgery ,surgical procedures, operative ,medicine.anatomical_structure ,Ventricle ,medicine.artery ,Internal medicine ,cardiovascular system ,medicine ,Aortic endothelium ,Cardiology ,cardiovascular diseases ,Heart valve ,business - Abstract
Objective: To design a novel percutaneous stented valve and model its implantation in the aorta.Background: The dimensions of stented aortic valve components govern its ability to prevent backflow of blood into the left ventricle. Whilst the theoretical parameters for the best stent performance have already been established, an effective valve model and its suitability along with the stent are lacking.Methods: This article discusses the design of a stented valve suitable for percutaneous aortic valve replacement. Steps involved in 3D CAD-based geometric modeling of the stented aortic valve and its implantation in the aorta are presented. Conceptual designing of individual components was used to build the total geometric model.Results: A novel geometric model of percutaneous stented aortic valve was generated. The improved design enhances its performance during and after implantation.Conclusion: The blunt hooks in the stent model prevent its migration in either direction by getting embedded in the aortic endothelium. This novel stent aortic valve may be of great interest to designers of future bioprosthetic heart valve models, as well as to surgeons involved in minimally invasive valve surgeries.
- Published
- 2010
35. Pten function in zebrafish
- Author
-
Suma Choorapoikayil, Miriam Stumpf, Jeroen den Hertog, and Hubrecht Institute for Developmental Biology and Stem Cell Research
- Subjects
PTEN ,animal structures ,Molecular Sequence Data ,Hemangiosarcoma ,AORTIC ENDOTHELIUM ,Review ,medicine.disease_cause ,Research Support ,General Biochemistry, Genetics and Molecular Biology ,TUMOR-SUPPRESSOR PTEN ,Animals, Genetically Modified ,Species Specificity ,medicine ,Journal Article ,Animals ,Humans ,HEMATOPOIETIC STEM-CELLS ,Amino Acid Sequence ,Progenitor cell ,Non-U.S. Gov't ,Molecular Biology ,Zebrafish ,ACUTE LYMPHOBLASTIC-LEUKEMIA ,Genetics ,biology ,LIPID PHOSPHATASE-ACTIVITY ,Tumor Suppressor Proteins ,Research Support, Non-U.S. Gov't ,PTEN Phosphohydrolase ,Wild type ,GERMLINE MUTATIONS ,Zebrafish Proteins ,biology.organism_classification ,Embryonic stem cell ,EMBRYONIC-DEVELOPMENT ,Cell biology ,Hematopoiesis ,Haematopoiesis ,TRANSGENIC ZEBRAFISH ,Lipid phosphatase activity ,Models, Animal ,embryonic structures ,biology.protein ,Angiogenesis ,SIGNALING PATHWAY ,CANCER SUSCEPTIBILITY ,Carcinogenesis - Abstract
Zebrafish is an excellent model system for the analysis of gene function. We and others use zebrafish to investigate the function of the tumor suppressor, Pten, in tumorigenesis and embryonic development. Zebrafish have two pten genes, ptena and ptenb. The recently identified N-terminal extension of human PTEN that may facilitate cell membrane transfer, appears not to be conserved in zebrafish Ptena or Ptenb. Mutants that retain a single wild type pten allele develop tumors, predominantly hemangiosarcomas. Homozygous double mutants are embryonic lethal. Zebrafish embryos lacking functional Pten display enhanced proliferation of endothelial cells, resulting in hyperbranching of blood vessels. In addition, ptena-/-ptenb-/- mutant embryos display enhanced proliferation of hematopoietic stem and progenitor cells and concomitant arrest of differentiation, although Pten-deficient cells commit to all blood cell lineages. Zebrafish is an ideal model for intravital imaging and future work using ptena-/-ptenb-/- mutants will enhance our understanding of the function of Pten in vivo. (C) 2014 Elsevier Inc. All rights reserved.
- Published
- 2014
36. Effect of Chronic Exercise and Angiotensin-Converting Enzyme Inhibition on Rodent Thoracic Aorta
- Author
-
Raymond Cartier, Martin G. Sirois, A. Couturier, Stéphane Elkouri, and Philippe Demers
- Subjects
Male ,Captopril ,Time Factors ,Rodent ,Drug Evaluation, Preclinical ,Administration, Oral ,Angiotensin-Converting Enzyme Inhibitors ,Aorta, Thoracic ,Blood Pressure ,Muscle, Smooth, Vascular ,Rats, Sprague-Dawley ,Phenylephrine ,Male rats ,Thoracic aorta ,biology ,medicine.diagnostic_test ,Chemistry ,Immunochemistry ,Heart ,Organ Size ,Up-Regulation ,Adenosine Diphosphate ,Vasodilation ,Aortic endothelium ,Cardiology and Cardiovascular Medicine ,Histamine ,medicine.drug ,medicine.medical_specialty ,Nitric Oxide Synthase Type III ,Blotting, Western ,Down-Regulation ,Drug Administration Schedule ,Vascular reactivity ,Western blot ,Physical Conditioning, Animal ,medicine.artery ,Internal medicine ,biology.animal ,von Willebrand Factor ,medicine ,Animals ,Pharmacology ,Ionophores ,Body Weight ,Angiotensin-converting enzyme ,Acetylcholine ,Rats ,Surgery ,Endocrinology ,biology.protein ,Calcium ,Endothelium, Vascular ,Nitric Oxide Synthase - Abstract
Vascular reactivity can be modulated by local physical factors as well as pharmacologic manipulations. The aim of this study was to evaluate the effects of chronic exercise (EX) with or without the ACEI captopril (CAP) on vascular reactivity. Sixty-four Sprague-Dawley male rats were randomized into 4 groups (n = 16): group 1, control; group 2, captopril; group 3, exercise; and group 4, exercise and captopril. After 10 weeks of treatment, rats were killed, and their thoracic aortas harvested. Vascular reactivity was studied in an organ chamber (n = 12). Aortic endothelium constitutive nitric oxyde synthase (NOS3) expression was determined by Western blot analysis (n = 4). Endothelial-dependent relaxation was increased in both CAP and EX rats relative to the control group. Maximal aortic relaxations were enhanced in the CAP group, and potencies of these mediators were enhanced in the EX group (P < 0.05 versus control). Combined treatment did not result in a synergistic effect. NOS3 relative expressions were: group 1, 100%; group 2, 241%; group 3, 64%; and group 4, 108%. Exercise enhanced both potencies and efficacies of the mediators studied, whereas CAP increased mainly their efficacies. NOS3 protein expression was up-regulated in CAP-treated rats but not in exercised rats. These findings suggest different mechanisms for the observed increased vascular reactivity.
- Published
- 2004
37. Functional implications of Ca2+ mobilizing properties for nitric oxide production in aortic endothelium
- Author
-
Tetsuya Koyama, Yushi Ito, Chiwaka Kimura, Sung Jin Park, and Masahiro Oike
- Subjects
Thapsigargin ,Aorta, Thoracic ,Stimulation ,Nitric Oxide ,General Biochemistry, Genetics and Molecular Biology ,Nitric oxide ,chemistry.chemical_compound ,Adenosine Triphosphate ,Extracellular ,Animals ,Enzyme Inhibitors ,General Pharmacology, Toxicology and Pharmaceutics ,Calcimycin ,Cells, Cultured ,Fluorescent Dyes ,Quenching (fluorescence) ,General Medicine ,Fluorescence ,chemistry ,Biochemistry ,Biophysics ,Aortic endothelium ,Calcium ,Cattle ,Fluorescein ,Endothelium, Vascular ,Intracellular - Abstract
We have investigated the relationship between Ca2+ mobilization and the cellular production of nitric oxide (NO) by using fura-2 and diaminofluorescein-2 (DAF-2), an NO-sensitive dye, in bovine aortic endothelial cells (BAEC). High concentrations of ATP (100 microM) or thapsigargin (1 micro M) depleted intracellular Ca2+ store sites with a single Ca2+ transient, and induced an increase in DAF-2 fluorescence even in Ca2+-free solution, thereby indicating that store depletion leads to NO production. The same level of increase in DAF-2 fluorescence was elicited by low concentrations of ATP (1 micro M), which induced Ca2+ oscillations but did not deplete store sites, only in the presence of extracellular Ca2+. Furthermore, inhibition of ATP (1 micro M)-induced Ca2+ entry with La3+ suppressed DAF-2 fluorescence. ATP (0.3 micro M), applied in Ca2+-free, Mn2+-containing solution induced Mn2+ entry-coupled fura-2 quenching, repeating shortly after each oscillation peak. These results indicate that NO is produced preferentially by entered Ca2+, and that Ca2+ oscillations, which are induced by low levels of stimulation, play a significant role in NO production by strongly modulating Ca2+ entry.
- Published
- 2002
38. Potential explanations for the French paradox
- Author
-
M.J. Patricia Mazier and Leasa L. Stanley
- Subjects
Wine ,Nutrition and Dietetics ,business.industry ,Endocrinology, Diabetes and Metabolism ,Saturated fat ,food and beverages ,medicine.disease ,Alcoholic beverage consumption ,Nitric oxide ,chemistry.chemical_compound ,Endocrinology ,High-density lipoprotein ,Biochemistry ,chemistry ,Hyperlipidemia ,medicine ,Aortic endothelium ,French paradox ,Food science ,business - Abstract
French total consumption of saturated fat is similar to that of other developed countries, while French mortality from coronary disease is only one third of the average. Since a distinguishing feature of the French diet is the regular consumption of red wine with meals, studies have focused on the correlation between alcoholic beverage consumption and the risk of coronary heart disease. This has been attributed to several factors: the ethanol itself, the phenols in wine, and a component in the grape skin which may be nitric oxide. Ethanol's cardioprotective effects may be due to its effect on the fibrinolytic factors or to high density lipoprotein concentrations. Phenols in red wine may act as antioxidants or may decrease thromboses. Finally, nitric oxide may relax aortic endothelium. In addition, it has been demonstrated that lower nitric oxide levels may lead to hyperlipidemia in rats. Overall, several wine components show promise for their possible cardiovascular protective effects. Caution, however, is required when formulating recommendations for daily alcohol consumption.
- Published
- 1999
39. Short-term parenteral application of α-tocopherol leads to increased concentration in plasma and tissues of the rat
- Author
-
Axel Jentzsch, Peter Fürst, Hans Konrad Biesalski, and Karin Engelhart
- Subjects
Male ,Parenteral Nutrition ,medicine.medical_specialty ,medicine.medical_treatment ,Ischemia ,Administration, Oral ,medicine.disease_cause ,Biochemistry ,High-performance liquid chromatography ,Placebos ,Rats, Sprague-Dawley ,chemistry.chemical_compound ,Internal medicine ,medicine ,Animals ,Vitamin E ,Lung ,Aorta ,business.industry ,General Medicine ,medicine.disease ,Rats ,Endocrinology ,medicine.anatomical_structure ,Liver ,chemistry ,Aortic endothelium ,Endothelium, Vascular ,alpha-Tocopherol ,business ,Oxidative stress - Abstract
Numerous studies suggest that supplemental vitamin E prior to or during vast surgeries might diminish or even prevent ischemia/reperfusion-induced injuries. In the present placebo-controlled study male Sprague-Dawley rats were supplemented parenterally or orally with alpha-tocopherol for three consecutive days. The applied amount of alpha-tocopherol was 2.3 micromol per day for oral and 1.2 micromol per day for parenteral supplementation. The enrichment of vitamin E concentrations in plasma and tissue samples (aortic endothelium, liver, and lung) was determined by HPLC. The vitamin E level was elevated following intravenous supplementation in plasma (21.4 +/- 1.9 micromol/L vs. 10.2 +/- 1.7 micromol/L in parenteral control group), in aortic endothelium (1.1 +/- 0.2 pmol/mm2 vs. 0.5 +/- 0.1 pmol/mm2) and in liver and lung (41.3 +/- 7.5 pmol/mg vs. 22.9 +/- 6.5 pmol/mg and 75.6 +/- 13.6 pmol/mg vs. 51.7 +/- 5.9 pmol/mg, respectively). Oral supplementation for three days also led to an increased level in liver (38.2 +/- 7.7 pmol/mg vs. 22.9 +/- 6.6 pmol/mg in oral control group) and in lung (67.8 +/- 5.7 pmol/mg vs. 51.7 +/- 9.3 pmol/mg) but not in aortic endothelium or plasma (0.8 +/- 0.3 pmol/mm2 vs. 0.6 +/- 0.3 pmol/mm2 and 12.0 +/- 2.2 micromol/L vs. 10.7 +/- 2.6 micromol/L).
- Published
- 1998
40. Hedgehog signaling via a calcitonin receptor-like receptor can induce arterial differentiation independently of VEGF signaling in zebrafish
- Author
-
Stefan Schulte-Merker, Philip W. Ingham, Roger Patient, Robert N. Wilkinson, Fredericus J.M. van Eeden, Marco J. Koudijs, and Hubrecht Institute for Developmental Biology and Stem Cell Research
- Subjects
Vascular Endothelial Growth Factor A ,Biochemistry ,hematopoietic stem-cells ,Animals, Genetically Modified ,chemistry.chemical_compound ,0302 clinical medicine ,endothelial-growth-factor ,Sonic hedgehog ,Experimental Zoology ,Zebrafish ,0303 health sciences ,Receptors, Notch ,Calcitonin Receptor-Like Protein ,Gene Expression Regulation, Developmental ,Hematology ,Arteries ,Hedgehog signaling pathway ,Cell biology ,Vascular endothelial growth factor ,Patched-1 Receptor ,Vascular endothelial growth factor A ,Gene Knockdown Techniques ,Core Binding Factor Alpha 2 Subunit ,Signal transduction ,notch ,Signal Transduction ,Patched Receptors ,medicine.medical_specialty ,kinase ,Immunology ,Notch signaling pathway ,Receptors, Cell Surface ,Biology ,Article ,aortic endothelium ,03 medical and health sciences ,blood ,Internal medicine ,medicine ,Animals ,Hedgehog Proteins ,gene ,Hedgehog ,030304 developmental biology ,pathway ,sonic-hedgehog ,Membrane Proteins ,Cell Biology ,CALCRL ,Zebrafish Proteins ,Hematopoietic Stem Cells ,Endocrinology ,chemistry ,Experimentele Zoologie ,Mutation ,biology.protein ,WIAS ,embryonic vascular development ,030217 neurology & neurosurgery - Abstract
Multiple signaling pathways control the specification of endothelial cells (ECs) to become arteries or veins during vertebrate embryogenesis. Current models propose that a cascade of Hedgehog (Hh), vascular endothelial growth factor (VEGF), and Notch signaling acts instructively on ECs to control the choice between arterial or venous fate. Differences in the phenotypes induced by Hh, VEGF, or Notch inhibition suggest that not all of the effects of Hh on arteriovenous specification are mediated by VEGF. We establish that full derepression of the Hh pathway in ptc1;ptc2 mutants converts the posterior cardinal vein into a second arterial vessel that manifests intact arterial gene expression, intersegmental vessel sprouting, and HSC gene expression. Importantly, although VEGF was thought to be absolutely essential for arterial fates, we find that normal and ectopic arterial differentiation can occur without VEGF signaling in ptc1;ptc2 mutants. Furthermore, Hh is able to bypass VEGF to induce arterial differentiation in ECs via the calcitonin receptor-like receptor, thus revealing a surprising complexity in the interplay between Hh and VEGF signaling during arteriovenous specification. Finally, our experiments establish a dual function of Hh during induction of runx1+ HSCs.
- Published
- 2012
41. Angiopoietin like‐2 stimulates leukocytes adhesion to the native aortic endothelium in LDLr−/−; hApoB100+/+ mice
- Author
-
Bruce G. Allen, Nada Farhat, Nathalie Thorin-Trescases, Louis Villeneuve, and Eric Thorin
- Subjects
Angiopoietin ,Chemistry ,LDL receptor ,Genetics ,Aortic endothelium ,Adhesion ,Molecular Biology ,Biochemistry ,Biotechnology ,Cell biology - Published
- 2012
42. X‐ray, proton and iron ion irradiation all increase adhesiveness of aortic endothelium and may accelerate development of atherosclerosis
- Author
-
Tao Yu, Kiran Gupta, Saman Khaled, Dennis F. Kucik, Polly Y. Chang, and Xing Wu
- Subjects
medicine.medical_specialty ,Proton ,Chemistry ,X-ray ,Biochemistry ,Ion ,Nuclear magnetic resonance ,Genetics ,medicine ,Aortic endothelium ,Irradiation ,Radiology ,Molecular Biology ,Biotechnology - Published
- 2010
43. Effects of Stent Design Parameters on the Aortic Endothelium
- Author
-
Lazar Mathew and Gideon Praveen Kumar
- Subjects
medicine.medical_specialty ,Aorta ,business.industry ,medicine.medical_treatment ,Large population ,Treatment method ,Stent ,Design team ,Valvular disease ,Internal medicine ,medicine.artery ,Aortic endothelium ,Cardiology ,Medicine ,business ,Stent design - Abstract
Vascular support structures are important tools for treating valve stenosis. A large population of patients is treated for valvular disease and the principal mode of treatment is the use of percutaneous valvuloplasty. Stent devices are proving to be an improved treatment method; these devices now account for 20% of treatments in Europe. This new technology provides highly effective results at minimal cost and short duration of hospitalization. Accurate and reliable structural analysis provides essential information to the design team in an environment where in vivo experimentation is extremely expensive, or impossible. This paper describes the design of vascular support structures (stents), to provide designers with estimates of the critical parameters which are essential to restore the functions of the endothelium of the Aorta during and after implantation without injuring it.
- Published
- 2009
44. Hedgehog signaling via a calcitonin receptor-like receptor can induce arterial differentiation independently of VEGF signaling in zebrafish
- Abstract
Multiple signaling pathways control the specification of endothelial cells (ECs) to become arteries or veins during vertebrate embryogenesis. Current models propose that a cascade of Hedgehog (Hh), vascular endothelial growth factor (VEGF), and Notch signaling acts instructively on ECs to control the choice between arterial or venous fate. Differences in the pheno-types induced by Hh, VEGF, or Notch inhibition suggest that not all of the effects of Hh on arteriovenous specification are mediated by VEGF. We establish that full derepression of the Hh pathway in ptc1;ptc2 mutants converts the posterior cardinal vein into a second arterial vessel that manifests intact arterial gene expression, intersegmental vessel sprouting, and HSC gene expression. Importantly, although VEGF was thought to be absolutely essential for arterial fates, we find that normal and ectopic arterial differentiation can occur without VEGF signaling in ptc1; ptc2 mutants. Furthermore, Hh is able to bypass VEGF to induce arterial differentiation in ECs via the calcitonin receptor-like receptor, thus revealing a surprising complexity in the interplay between Hh and VEGF signaling during arteriovenous specification. Finally, our experiments establish a dual function of Hh during induction of runx1(+) HSCs. (Blood. 2012;120(2):477-488)
- Published
- 2012
45. Triglyceride‐rich lipoproteins prime aortic endothelium for an enhanced inflammatory response to TNF‐α
- Author
-
Anne A Knowlton, Harold J. Ting, Anthony G. Passerini, and Scott I. Simon
- Subjects
medicine.medical_specialty ,Triglyceride ,business.industry ,Inflammatory response ,Biochemistry ,Prime (order theory) ,chemistry.chemical_compound ,Endocrinology ,chemistry ,Internal medicine ,Genetics ,medicine ,Aortic endothelium ,Tumor necrosis factor alpha ,business ,Molecular Biology ,Biotechnology - Published
- 2007
46. Twenty-fold difference in hemodynamic wall shear stress between murine and human aortas
- Author
-
C. Ross Ethier and Peter D. Weinberg
- Subjects
Endothelium ,Rehabilitation ,Body Weight ,Biomedical Engineering ,Biophysics ,Vascular biology ,Hemodynamics ,Anatomy ,Aortic flow ,Biology ,Vascular tone ,Biomechanical Phenomena ,medicine.anatomical_structure ,Species Specificity ,cardiovascular system ,medicine ,Shear stress ,Aortic endothelium ,Animals ,Humans ,Orthopedics and Sports Medicine ,Endothelium, Vascular ,Stress, Mechanical ,Aorta - Abstract
Endothelial cells regulate vascular tone and mural remodelling in a shear-dependent manner that is commonly assumed to keep wall shear stress constant across arteries and species. Allometric arguments show that aortic flow velocity is constant across species, a deduction that is consistent with much experimental data, but the same arguments also show that the shear stress experienced by aortic endothelium will depend inversely on body mass to the 3 8 th power, and hence will be 20-fold higher in mice than in men. This conclusion is robust and has important implications for the study of shear-dependent vascular biology and pathology.
- Published
- 2006
47. Binding of triglyceride rich lipoproteins to LDL receptor amplifies inflammatory responses of aortic endothelium
- Author
-
Andrew F. Powers, Scott I. Simon, John C. Rutledge, and Harold J. Ting
- Subjects
medicine.medical_specialty ,chemistry.chemical_compound ,Endocrinology ,Triglyceride ,Chemistry ,Internal medicine ,LDL receptor ,Genetics ,Aortic endothelium ,medicine ,Molecular Biology ,Biochemistry ,Biotechnology - Published
- 2006
48. Are intra-aortic hemopoietic cells derived from endothelial cells during ontogeny?
- Author
-
Thierry Jaffredo, Karine Bollerot, Claire Pouget, and Françoise Dieterlen-Lièvre
- Subjects
Aorta ,Ontogeny ,Avian embryo ,Anatomy ,Biology ,Hematopoietic Stem Cells ,Cell biology ,Haematopoiesis ,medicine.artery ,cardiovascular system ,medicine ,Aortic endothelium ,Animals ,Endothelium, Vascular ,Stem cell ,Cardiology and Cardiovascular Medicine ,Cells, Cultured - Abstract
The aorta is recognized as an intraembryonic site that produces adult-type hemopoietic stem cells. A corpus of data indicates that hemopoietic cells arranged as clusters attached to the aortic floor derive from an endothelial intermediate. This review reports on experimental approaches carried out in the avian embryo to establish the developmental history of the aortic endothelium and trace the origin of associated hemopoietic cells.
- Published
- 2005
49. Ultrastructural investigations on protective effects of NCX 4016 (nitroaspirin) on macrovascular endothelium in diabetic Wistar rats
- Author
-
Ambrosini, Maria Vittoria, Mariucci, Giuseppina, Rambotti, Maria Grazia, Tantucci, M., Covarelli, C., De Angelis, L., and Fiorucci, Stefano
- Subjects
nitric oxide-donating aspirin ,diabetes ,NCX 4016 ,transmission electron microscopy ,rat ,Aortic endothelium ,scanning electron microscopy - Published
- 2005
50. Effect of thiazolidinediones and metformin on LDL oxidation and aortic endothelium relaxation in diabetic GK rats
- Author
-
Katsuo Kamata, Hideo Toyoshima, Yoshitaka Iwama, Kaoruko Tada Iida, Hirohito Sone, Yoshiro Watanabe, Hitoshi Shimano, Yasushi Kawakami, Masatsune Suzuki, Kazunori Shimada, Nobuhiro Yamada, and Hiroshi Mokuno
- Subjects
Male ,medicine.medical_specialty ,Physiology ,Arteriosclerosis ,Endocrinology, Diabetes and Metabolism ,medicine.medical_treatment ,Muscle Relaxation ,Vasodilator Agents ,Aorta, Thoracic ,Troglitazone ,Lipid oxidation ,Physiology (medical) ,Internal medicine ,Isometric Contraction ,medicine ,Animals ,Hypoglycemic Agents ,Chromans ,Rats, Wistar ,Relaxation (psychology) ,Pioglitazone ,business.industry ,Insulin ,Cholesterol, LDL ,Lipids ,Acetylcholine ,Metformin ,Rats ,Thiazoles ,Endocrinology ,Diabetes Mellitus, Type 2 ,Aortic endothelium ,Thiazolidinediones ,Endothelium, Vascular ,Lipid Peroxidation ,business ,Oxidation-Reduction ,medicine.drug ,Muscle Contraction - Abstract
In this study, using GK diabetic rats, we compared the effects of three insulin sensitizers on lipid oxidation and the aortic relaxation response. Eight-week-old rats were treated for 4 wk with either troglitazone or pioglitazone, both of which are thiazolidinediones, or with metformin. Despite the fact that only troglitazone has a similarity in structure to α-tocopherol, a potent antioxidant, the level of thiobarbituric acid-reactive substance was lower, and the lag time of the conjugated dienes was longer, in the blood samples from the rats in both troglitazone- and pioglitazone-treated groups. In contrast, another insulin sensitizer, metformin, failed to inhibit the oxidation of blood samples. The aortic vasorelaxation response was increased in both troglitazone- and metformin-treated groups compared with the untreated group. These findings suggest that thiazolidinediones have a beneficial effect on lipid oxidation irrespective of the drug's structural similarity to α-tocopherol. It is also suggested that the thiazolidinediones and metformin improve vascular function in diabetes. These effects may play a role in the prevention of atherosclerosis in diabetic patients.
- Published
- 2003
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