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Surgical vein graft preparation promotes cellular dysfunction, oxidative stress, and intimal hyperplasia in human saphenous vein.
Osgood MJ, Hocking KM, Voskresensky IV, Li FD, Komalavilas P, Cheung-Flynn J, Brophy CM
(2014) J Vasc Surg 60: 202-11
MeSH Terms: Aged, Endothelium, Vascular, Female, Humans, Hydrogen Peroxide, Hyperplasia, Male, Middle Aged, Muscle, Smooth, Vascular, Nitric Oxide Synthase, Organ Culture Techniques, Oxidative Stress, Platelet Endothelial Cell Adhesion Molecule-1, Reactive Oxygen Species, Saphenous Vein, Time Factors, Tunica Intima, Vascular Surgical Procedures, Warm Ischemia
Show Abstract · Added March 9, 2015
INTRODUCTION - Human saphenous vein (HSV) is the most widely used bypass conduit for peripheral and coronary vascular reconstructions. However, outcomes are limited by a high rate of intimal hyperplasia (IH). HSV undergoes a series of ex vivo surgical manipulations prior to implantation, including hydrostatic distension, marking, and warm ischemia in solution. We investigated the impact of surgical preparation on HSV cellular function and development of IH in organ culture. We hypothesized that oxidative stress is a mediator of HSV dysfunction.
METHODS - HSV was collected from patients undergoing vascular bypass before and after surgical preparation. Smooth muscle and endothelial function were measured using a muscle bath. Endothelial preservation was assessed with immunohistochemical staining. An organ culture model was used to investigate the influence of surgical preparation injury on the development of IH. Superoxide levels were measured using a high-performance liquid chromatography-based assay. The influence of oxidative stress on HSV physiologic responses was investigated by exposing HSV to hydrogen peroxide (H2O2).
RESULTS - Surgical vein graft preparation resulted in smooth muscle and endothelial dysfunction, endothelial denudation, diminished endothelial nitric oxide synthase staining, development of increased IH, and increased levels of reactive oxygen species. Experimental induction of oxidative stress in unmanipulated HSV by treatment with H2O2 promoted endothelial dysfunction. Duration of storage time in solution did not contribute to smooth muscle or endothelial dysfunction.
CONCLUSIONS - Surgical vein graft preparation causes dysfunction of the smooth muscle and endothelium, endothelial denudation, reduced endothelial nitric oxide synthase expression, and promotes IH in organ culture. Moreover, increased levels of reactive oxygen species are produced and may promote further vein graft dysfunction. These results argue for less injurious means of preparing HSV prior to autologous transplantation into the arterial circulation.
Copyright © 2014 Society for Vascular Surgery. All rights reserved.
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19 MeSH Terms
Adenosine A2B receptors on cardiac stem cell antigen (Sca)-1-positive stromal cells play a protective role in myocardial infarction.
Ryzhov S, Zhang Q, Biaggioni I, Feoktistov I
(2013) Am J Pathol 183: 665-72
MeSH Terms: Animals, Antigens, Ly, Cardiotonic Agents, Heart Function Tests, Membrane Proteins, Mesenchymal Stem Cell Transplantation, Mice, Mice, Inbred C57BL, Mice, Knockout, Myocardial Infarction, Myocardium, Platelet Endothelial Cell Adhesion Molecule-1, Receptor, Adenosine A2B, Signal Transduction, Stromal Cells, Survival Analysis
Show Abstract · Added May 29, 2014
Transplantation of mesenchymal stem-like cells to the heart is known to improve cardiac recovery in animal models of myocardial infarction (MI). Because stimulation of A2B adenosine receptors on mouse cardiac stem cell antigen (Sca)-1(+)CD31(-) mesenchymal stem-like cells significantly up-regulates their secretion of pro-angiogenic factors, we hypothesized that ablation of the A2B receptor signaling in these cells would reduce their ability to improve vascularization of the infarct area seen after transplantation. Wild-type (WT) C57BL/6 mice underwent permanent left coronary artery ligation and received intramyocardial injections of Sca-1(+)CD31(-) cells generated from WT or A2B receptor knockout (A2BKO) mice or the same volume of cell-free saline. Only 12% to 16% of injected cells remained in the ventricles 1 week later; there was no significant difference between WT and A2BKO cell survival. Transplantation of WT, but not A2BKO, cells significantly reduced both post-MI decline in cardiac function and adverse remodeling compared with that seen in control hearts. Morphological analysis conducted 4 weeks after MI revealed significantly increased vascularization of the infarct areas and reduced myocardial scarring in animals treated with WT, but not with A2BKO, cells compared with control. Thus, our study demonstrated that the A2B receptor signaling linked to up-regulation of pro-angiogenic factors in cardiac Sca-1(+)CD31(-) stromal cells is essential for overall improvement of cardiac recovery seen after their transplantation to the injured heart.
Copyright © 2013 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.
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16 MeSH Terms
Circulating CD31+ leukocyte frequency is associated with cardiovascular risk factors.
Ge Y, Cheng S, Larson MG, Ghorbani A, Martin RP, Klein RJ, O'Donnell CJ, Vasan RS, Shaw SY, Wang TJ, Cohen KS
(2013) Atherosclerosis 229: 228-33
MeSH Terms: Aged, Cardiovascular Diseases, Endothelial Cells, Female, Flow Cytometry, Humans, Immunophenotyping, Leukocyte Count, Leukocytes, Longitudinal Studies, Male, Middle Aged, Platelet Endothelial Cell Adhesion Molecule-1, Risk Factors
Show Abstract · Added April 15, 2014
OBJECTIVES - CD31 identifies a heterogeneous population of cells in the blood, consisting of mature leukocytes and platelets, as well as smaller numbers of endothelial and progenitor cells. Because unfractionated CD31+ blood cells have demonstrated angiogenic properties in vivo, we hypothesized that circulating CD31+ cells would be related to the presence of cardiovascular risk factors in humans.
METHODS AND RESULTS - We studied 1487 participants, free of cardiovascular disease, from the Framingham Offspring Study. Using anti-human CD31 and CD45 antibodies, distinct CD31+/CD45+ leukocyte populations were enumerated in blood samples by FACS analysis. We used linear regression analyses to investigate the relation of each cell phenotype with cardiovascular risk factors. We identified 3 distinct leukocyte populations: CD31-, CD31 dim, and CD31 bright cells. Using forward/side scatter analyses, CD31- and CD31 dim cells mapped to lymphoid gates while CD31 bright cells were monocytoid. In multivariable analyses, higher frequency of CD31 bright cells was associated with older age, male sex, HDL cholesterol, and CRP (all P < 0.01). In contrast, CD31 dim was inversely associated with age, male sex, CRP, and smoking (all P < 0.01). Framingham Risk Score was positively associated with CD31 bright frequency (P = 0.002), and negatively associated with CD31 dim frequency (P = 0.020).
CONCLUSIONS - CD31+ staining identifies 2 major leukocyte populations, CD31 bright and CD31 dim, which demonstrated significant and opposite associations with cardiovascular risk in humans. Further research is needed to define the biological and potential therapeutic roles of CD31+ subpopulations in vascular disease.
Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.
0 Communities
1 Members
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14 MeSH Terms
Sonic Hedgehog contributes to gastric mucosal restitution after injury.
Xiao C, Feng R, Engevik AC, Martin JR, Tritschler JA, Schumacher M, Koncar R, Roland J, Nam KT, Goldenring JR, Zavros Y
(2013) Lab Invest 93: 96-111
MeSH Terms: Animals, Carrier Proteins, Gastric Mucosa, Hedgehog Proteins, Kruppel-Like Transcription Factors, Macrophages, Membrane Glycoproteins, Mice, Mice, Knockout, Platelet Endothelial Cell Adhesion Molecule-1, RNA, Messenger, Stomach Ulcer, Tamoxifen, Vascular Endothelial Growth Factor A, Wound Healing, Zinc Finger Protein GLI1
Show Abstract · Added September 3, 2013
Eradication of Helicobacter pylori correlates with regeneration of the gastric epithelium, ulcer healing and re-expression of the gastric morphogen Sonic Hedgehog (Shh). We sought to identify the role of Shh as a regulator of gastric epithelial regeneration during wound healing. A mouse model expressing a parietal cell-specific, tamoxifen-inducible deletion of Shh (HKCre(ERT2);Shh(flox/flox) or PC-iShhKO) was developed. Stomachs were collected and compared 7-150 days after the final vehicle or tamoxifen injection. Ulcers were induced in both controls and PC-iShhKO mice using acetic acid and ulcer size compared 1 and 7 days post induction. (1) Re-expression of Shh correlates with decreased hyperproliferation: Compared to controls, PC-iShhKO mice developed foveolar hyperplasia. Restoration of normal gastric epithelial architecture and differentiation correlated with the re-expression of Shh in PC-iShhKO mice 150 days after the final tamoxifen injection. At the tamoxifen dose used to induce Cre recombination there was no genotoxicity reported in either HKCre(ERT2) or Shh(flox/flox) control mouse stomachs. (2) Delayed wound healing in PC-iShhKO mouse stomachs: To identify the role of Shh in gastric regeneration, an acetic acid ulcer was induced in control and PC-iShhKO mice. Ulcers began to heal in control mice by 7 days after induction. Ulcer healing was documented by decreased ulcer size, angiogenesis, macrophage infiltration and formation of granulation tissue that correlated with the re-expression of Shh within the ulcerated tissue. PC-iShhKO mice did not show evidence of ulcer healing. Re-expression of Shh contributes to gastric regeneration. Our current study may have clinical implications given that eradication of H. pylori correlates with re-expression of Shh, regeneration of the gastric epithelium and ulcer healing.
2 Communities
3 Members
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16 MeSH Terms
Role of A2B adenosine receptors in regulation of paracrine functions of stem cell antigen 1-positive cardiac stromal cells.
Ryzhov S, Goldstein AE, Novitskiy SV, Blackburn MR, Biaggioni I, Feoktistov I
(2012) J Pharmacol Exp Ther 341: 764-74
MeSH Terms: Adenosine, Adenosine Deaminase, Agammaglobulinemia, Animals, Antigens, Ly, Cells, Cultured, Chemokine CXCL1, Female, Interleukin-6, Male, Membrane Proteins, Mesenchymal Stem Cells, Mice, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Myocardial Infarction, Myocardium, Paracrine Communication, Platelet Endothelial Cell Adhesion Molecule-1, RNA, Messenger, Receptor, Adenosine A2B, Severe Combined Immunodeficiency, Stem Cells, Up-Regulation, Vascular Endothelial Growth Factor A
Show Abstract · Added May 29, 2014
The existence of multipotent cardiac stromal cells expressing stem cell antigen (Sca)-1 has been reported, and their proangiogenic properties have been demonstrated in myocardial infarction models. In this study, we tested the hypothesis that stimulation of adenosine receptors on cardiac Sca-1(+) cells up-regulates their secretion of proangiogenic factors. We found that Sca-1 is expressed in subsets of mouse cardiac stromal CD31(-) and endothelial CD31(+) cells. The population of Sca-1(+)CD31(+) endothelial cells was significantly reduced, whereas the population of Sca-1(+)CD31(-) stromal cells was increased 1 week after myocardial infarction, indicating their relative functional importance in this pathophysiological process. An increase in adenosine levels in adenosine deaminase-deficient mice in vivo significantly augmented vascular endothelial growth factor (VEGF) production in cardiac Sca-1(+)CD31(-) stromal cells but not in Sca-1(+)CD31(+) endothelial cells. We found that mouse cardiac Sca-1(+)CD31(-) stromal cells predominantly express mRNA encoding A(2B) adenosine receptors. Stimulation of adenosine receptors significantly increased interleukin (IL)-6, CXCL1 (a mouse ortholog of human IL-8), and VEGF release from these cells. Using conditionally immortalized Sca-1(+)CD31(-) stromal cells obtained from wild-type and A(2B) receptor knockout mouse hearts, we demonstrated that A(2B) receptors are essential for adenosine-dependent up-regulation of their paracrine functions. We found that the human heart also harbors a population of stromal cells similar to the mouse cardiac Sca-1(+)CD31(-) stromal cells that increase release of IL-6, IL-8, and VEGF in response to A(2B) receptor stimulation. Thus, our study identified A(2B) adenosine receptors on cardiac stromal cells as potential targets for up-regulation of proangiogenic factors in the ischemic heart.
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26 MeSH Terms
Utility of immunohistochemical staining with FLI1, D2-40, CD31, and CD34 in the diagnosis of acquired immunodeficiency syndrome-related and non-acquired immunodeficiency syndrome-related Kaposi sarcoma.
Rosado FG, Itani DM, Coffin CM, Cates JM
(2012) Arch Pathol Lab Med 136: 301-4
MeSH Terms: Acquired Immunodeficiency Syndrome, Antibodies, Monoclonal, Murine-Derived, Antigens, CD34, Biomarkers, Tumor, Diagnosis, Differential, Disease Progression, Humans, Immunohistochemistry, Neoplasm Staging, Platelet Endothelial Cell Adhesion Molecule-1, Proto-Oncogene Protein c-fli-1, Reproducibility of Results, Retrospective Studies, Sarcoma, Kaposi, Sensitivity and Specificity, Staining and Labeling
Show Abstract · Added March 15, 2013
CONTEXT - Kaposi sarcoma (KS) is a vascular tumor frequently associated with advanced human immunodeficiency virus infection, advanced age, or iatrogenic immunosuppression. Immunohistochemistry for CD31 and CD34, and more recently for FLI1 and D2-40, has been used as ancillary diagnostic tests for KS, despite little information regarding the sensitivities and differential staining patterns of the latter 2 markers in the major clinical subtypes and histologic stages of KS.
OBJECTIVE - This retrospective study aims to assess the prevalence of the vascular markers D2-40 and FLI1 in the main clinical subgroups and tumor stages of KS.
DESIGN - Twenty-four cases of KS (12 acquired immunodeficiency syndrome [AIDS]-related cases and 12 non-AIDS-related cases; 11 nodular-stage and 13 patch/plaque-stage KS) were stained for CD34, CD31, D2-40, and FLI1 by immunohistochemistry. The distribution of immunoreactivity was compared between the clinical subtypes and tumor stages of KS using the Mann-Whitney test.
RESULTS - CD31, CD34, D2-40, and FLI1 strongly and diffusely stained tumor cells in 75%, 92%, 67%, and 92% of AIDS-related cases and 58%, 92%, 67%, and 75% of non-AIDS-related cases, respectively. Differences in the proportions of positive cases between AIDS-related and non-AIDS-related cases did not reach statistical significance. No significant staining differences were observed between nodular- and patch/plaque-stage KS either.
CONCLUSIONS - There are no differences in the distribution of immunohistochemical reactivity for CD31, CD34, D2-40, or FLI1 between AIDS-related and non-AIDS-related KS or between nodular- and patch/plaque-stage KS. All of the markers studied demonstrated high sensitivity in both clinical settings and both stages of tumor progression.
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1 Members
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16 MeSH Terms
TGF-β sequestration by mesangial cell integrin αvβ8: A novel mechanism of glomerular endothelial cell regulation.
Pozzi A, Zent R
(2011) Am J Pathol 178: 485-9
MeSH Terms: Animals, Endothelial Cells, Integrins, Mesangial Cells, Mice, Models, Biological, Platelet Endothelial Cell Adhesion Molecule-1, Transforming Growth Factor beta
Added February 24, 2014
1 Communities
2 Members
1 Resources
8 MeSH Terms
6-Mercaptopurine, monocytes, and atherosclerosis.
Linton MF, Fazio S
(2010) Arterioscler Thromb Vasc Biol 30: 1494-6
MeSH Terms: Animals, Apolipoprotein E3, Apoptosis, Atherosclerosis, Cell Adhesion, Chemokine CCL2, Chemotaxis, Humans, Immunosuppressive Agents, Inflammation Mediators, Integrin alpha4beta1, Macrophages, Mercaptopurine, Mice, Monocytes, Platelet Endothelial Cell Adhesion Molecule-1, Proto-Oncogene Proteins c-bcl-2, bcl-X Protein
Added May 27, 2014
0 Communities
1 Members
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18 MeSH Terms
VHL and PTEN loss coordinate to promote mouse liver vascular lesions.
Chen S, Sanford CA, Sun J, Choi V, Van Dyke T, Samulski RJ, Rathmell WK
(2010) Angiogenesis 13: 59-69
MeSH Terms: Animals, Cell Proliferation, Dependovirus, Gene Deletion, Gene Transfer Techniques, Humans, Hypoxia-Inducible Factor 1, alpha Subunit, Immunohistochemistry, Injections, Intravenous, Lipid Metabolism, Liver, Mice, PTEN Phosphohydrolase, Phosphorylation, Platelet Endothelial Cell Adhesion Molecule-1, Proto-Oncogene Proteins c-akt, Recombination, Genetic, Up-Regulation, Vascular Diseases, Vascular Endothelial Growth Factor A, Von Hippel-Lindau Tumor Suppressor Protein
Show Abstract · Added October 17, 2015
Von Hippel-Lindau (VHL) inactivation develops a tumor syndrome characterized by highly vascularized tumors as a result of hypoxia inducible factors (HIF) stabilization. The most common manifestation is the development of hemangioblastomas typically located in the central nervous system and other organs including the liver. PTEN (Phosphatase and tension homologue deleted on chromosome 10) inactivation also upregulates HIF-1alpha and may take part in promoting vascular lesions in tumors. The coordinate effect of loss of these tumor suppressors on HIF levels, and the subsequent effect on vascular lesion formation would elucidate the potential for mechanisms to modify HIF dosage supplementally and impact tumor phenotype. We therefore employed models of somatic conditional inactivation of Vhl, Pten, or both tumor suppressor genes in individual cells of the liver by Cre-loxP recombination to study the cooperativity of these two tumor suppressors in preventing tumor formation. Nine months after tumor suppressor inactivation, Vhl conditional deletion (Vhl (loxP/loxP)) mice showed no abnormalities, Pten conditional deletion (Pten (loxP/loxP)) mice developed liver steatosis and focal nodular expansion of hepatocytes containing lipid droplet and fat. Vhl and Pten conditional deletion (Vhl (loxP/loxP);Pten (loxP/loxP)) mice, however, developed multiple cavernous liver lesions reminiscent of hemangioblastoma. Liver hemangioblastomas in VHL disease may, therefore, require secondary mutation in addition to VHL loss of heterozygosity which is permissive for vascular lesion development or augments levels of HIF-1alpha.
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1 Members
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21 MeSH Terms
Levels of endocannabinoids and palmitoylethanolamide and their pharmacological manipulation in chronic granulomatous inflammation in rats.
Endocannabinoid Research Group, De Filippis D, D'Amico A, Cipriano M, Petrosino S, Orlando P, Di Marzo V, Iuvone T
(2010) Pharmacol Res 61: 321-8
MeSH Terms: Amidohydrolases, Animals, Arachidonic Acids, Cannabinoid Receptor Modulators, Carrageenan, Chronic Disease, Disease Models, Animal, Dose-Response Relationship, Drug, Endocannabinoids, Ethanolamines, Granuloma, Hemoglobins, Inflammation, Male, Neovascularization, Pathologic, Palmitic Acids, Phospholipase D, Platelet Endothelial Cell Adhesion Molecule-1, Rats, Rats, Wistar, Receptors, Cannabinoid, Serotonin, TRPV Cation Channels
Show Abstract · Added April 10, 2014
The endocannabinoids anandamide and 2-arachidonoylglycerol, and the anandamide-congener, palmitoylethanolamide, are all substrates for the enzyme fatty acid amide hydrolase, and are endowed with anti-inflammatory actions exerted via cannabinoid receptors or, in the case of palmitoylethanolamide, also via other targets. We investigated the role of the endocannabinoid system during granuloma formation, a model of chronic inflammation sustained by neoangiogenesis, in rats. Granuloma was induced by subcutaneous lambda-carrageenin-soaked sponge implants on the back of male Wistar rats. After 96h, granulomas were detached and tissue formation was evaluated as wet weight; the endocannabinoid system was evaluated by the measurement of endocannabinoid levels, by LC-MS, and of cannabinoid receptor expression, by western blot analysis. Moreover, angiogenesis was evaluated by the measurement of both hemoglobin content and CD31 protein expression. Arachidonoylserotonin (AA-5-HT, 12.5-50mug/ml), an inhibitor of FAAH, and palmitoylethanolamide (PEA, 200-800mug/ml) were given locally only once at the time of implantation. Granuloma formation was accompanied by a significant decrease in endocannabinoid and palmitoylethanolamide levels paralleled by increased levels of the fatty acid amide hydrolase, responsible for their breakdown. Moreover, an increase of cannabinoid receptor expression was also observed. Pharmacological elevation of endocannabinoids and palmitoylethanolamide, obtained separately by arachidonoylserotonin and exogenous palmitoylethanolamide treatment, dose-dependently reduced inflammatory hallmarks including tumor necrosis factor-alpha as well as granuloma-dependent angiogenesis. The effect of arachidonoylserotonin was accompanied by near-normalization of 2-arachidonoylglycerol and palmitoylethanolamide levels in the tissue. These findings suggest that chronic inflammation might develop also because of endocannabinoid and palmitoylethanolamide tissue concentration impairment, the correction of which might be exploited to develop new anti-inflammatory drugs.
Copyright 2009 Elsevier Ltd. All rights reserved.
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23 MeSH Terms