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Schuchardt, M., primary, Toelle, M., additional, Huang, T., additional, Wiedon, A., additional, Van Der Giet, M., additional, Mill, C., additional, George, S., additional, Jeremy, J., additional, Santulli, G., additional, Illario, M., additional, Cipolletta, E., additional, Sorriento, D., additional, Del Giudice, C., additional, Anastasio, A., additional, Trimarco, B., additional, Iaccarino, G., additional, Jobs, A., additional, Wagner, C., additional, Kurtz, A., additional, De Wit, C., additional, Koller, A., additional, Suvorava, T., additional, Weber, M., additional, Dao, V., additional, Kojda, G., additional, Tsaousi, A., additional, Lyon, C., additional, Williams, H., additional, Barth, N., additional, Loot, A., additional, Fleming, I., additional, Keul, P., additional, Lucke, S., additional, Graeler, M., additional, Heusch, G., additional, Levkau, B., additional, Biessen, E., additional, De Jager, S., additional, Bermudez-Pulgarin, B., additional, Bot, I., additional, Abia, R., additional, Van Berkel, T., additional, Renger, A., additional, Noack, C., additional, Zafiriou, M., additional, Dietz, R., additional, Bergmann, M., additional, Zelarayan, L., additional, Hammond, J., additional, Hamelet, J., additional, Van Assche, T., additional, Belge, C., additional, Vanderper, A., additional, Langin, D., additional, Herijgers, P., additional, Balligand, J., additional, Perrot, A., additional, Neubert, M., additional, Posch, M., additional, Oezcelik, C., additional, Waldmuller, S., additional, Berger, F., additional, Scheffold, T., additional, Bouvagnet, P., additional, Ozcelik, C., additional, Lebreiro, A., additional, Martins, E., additional, Lourenco, P., additional, Cruz, C., additional, Martins, M., additional, Bettencourt, P., additional, Maciel, M., additional, Abreu-Lima, C., additional, Pilichou, K., additional, Bauce, B., additional, Rampazzo, A., additional, Carturan, E., additional, Corrado, D., additional, Thiene, G., additional, Basso, C., additional, Piccini, I., additional, Fortmueller, L., additional, Kuhlmann, M., additional, Schaefers, M., additional, Carmeliet, P., additional, Kirchhof, P., additional, Fabritz, L., additional, Sanchez, J., additional, Rodriguez-Sinovas, A., additional, Agullo, E., additional, Garcia-Dorado, D., additional, Lymperopoulos, A., additional, Rengo, G., additional, Gao, E., additional, Zincarelli, C., additional, Koch, W., additional, Morgan, P., additional, Diez, A., additional, Perez, N., additional, Cingolani, H., additional, Zahradnikova, A., additional, Polakova, E., additional, Zahradnik, I., additional, Fluschnik, N., additional, Sossalla, S., additional, Ort, K., additional, Neef, S., additional, Hasenfuss, G., additional, Maier, L., additional, Weinert, S., additional, Poitz, D., additional, Herold, J., additional, Schmeisser, A., additional, Strasser, J., additional, Braun-Dullaeus, R., additional, Nazari-Jahantigh, M., additional, Weber, C., additional, Schober, A., additional, Leuner, A., additional, Eichhorn, B., additional, Ravens, U., additional, Morawietz, H., additional, Babes, E., additional, Babes, V., additional, Popescu, M., additional, Ardelean, A., additional, Rus, M., additional, Bustea, C., additional, Gwozdz, P., additional, Csanyi, G., additional, Luzak, B., additional, Gajda, M., additional, Mateuszuk, L., additional, Chmura-Skirlinska, A., additional, Watala, C., additional, Chlopicki, S., additional, Kierzkowska, I., additional, Sulicka, J., additional, Kwater, A., additional, Strach, M., additional, Surdacki, A., additional, Siedlar, M., additional, Grodzicki, T., additional, Olieslagers, S., additional, Pardali, L., additional, Tchaikovski, V., additional, Ten Dijke, P., additional, Waltenberger, J., additional, Renner, M., additional, Redwan, B., additional, Winter, M., additional, Panzenboeck, A., additional, Jakowitsch, J., additional, Sadushi-Kolici, R., additional, Bonderman, D., additional, Lang, I., additional, Toso, A., additional, Tanini, L., additional, Pizzetti, T., additional, Leoncini, M., additional, Maioli, M., additional, Tedeschi, D., additional, Oliviero, C., additional, Bellandi, F., additional, Casprini, P., additional, Amato, M., additional, Molins, B., additional, Pena, E., additional, Badimon, L., additional, Ferreiro Gutierrez, J., additional, Ueno, M., additional, Alissa, R., additional, Dharmashankar, K., additional, Capodanno, D., additional, Desai, B., additional, Bass, T., additional, Angiolillo, D., additional, Chabielska, E., additional, Gromotowicz, A., additional, Szemraj, J., additional, Stankiewicz, A., additional, Zakrzeska, A., additional, Mohammed, S., additional, Molla, F., additional, Soldo, A., additional, Russo, I., additional, Germano, G., additional, Balconi, G., additional, Staszewsky, L., additional, Latini, R., additional, Lynch, F., additional, Austin, C., additional, Prendergast, B., additional, Keenan, D., additional, Malik, R., additional, Izzard, A., additional, Heagerty, A., additional, Czikora, A., additional, Lizanecz, E., additional, Rutkai, I., additional, Boczan, J., additional, Porszasz, R., additional, Papp, Z., additional, Edes, I., additional, Toth, A., additional, Colantuoni, A., additional, Vagnani, S., additional, Lapi, D., additional, Maroz-Vadalazhskaya, N., additional, Koslov, I., additional, Shumavetz, V., additional, Glibovskaya, T., additional, Ostrovskiy, Y., additional, Koutsiaris, A., additional, Tachmitzi, S., additional, Kotoula, M., additional, Giannoukas, A., additional, Tsironi, E., additional, Darago, A., additional, Orosz, P., additional, Megyesi, Z., additional, Schudeja, S., additional, Matschke, K., additional, Deussen, A., additional, Castro, M., additional, Cena, J., additional, Walsh, M., additional, Schulz, R., additional, Poddar, K., additional, Rha, S., additional, Ramasamy, S., additional, Park, J., additional, Choi, C., additional, Seo, H., additional, Park, C., additional, Oh, D., additional, Almeida, J., additional, Pimenta, S., additional, Bernardes, J., additional, Machado, J., additional, Sabatasso, S., additional, Laissue, J., additional, Hlushchuk, R., additional, Brauer-Krisch, E., additional, Bravin, A., additional, Blattmann, H., additional, Michaud, K., additional, Djonov, V., additional, Hirschberg, K., additional, Tarcea, V., additional, Pali, S., additional, Korkmaz, S., additional, Loganathan, S., additional, Merkely, B., additional, Karck, M., additional, Szabo, G., additional, Pagliani, L., additional, Faggin, E., additional, Rattazzi, M., additional, Puato, M., additional, Presta, M., additional, Grego, F., additional, Deriu, G., additional, Pauletto, P., additional, Kaiser, R., additional, Albrecht, K., additional, Schgoer, W., additional, Theurl, M., additional, Beer, A., additional, Wiedemann, D., additional, Steger, C., additional, Bonaros, N., additional, Kirchmair, R., additional, Kharlamov, A., additional, Cabaravdic, M., additional, Breuss, J., additional, Uhrin, P., additional, Binder, B., additional, Fiordaliso, F., additional, Maggioni, M., additional, Biondi, A., additional, Masson, S., additional, Cervo, L., additional, Francke, A., additional, Soenke, W., additional, Strasser, R., additional, Hecht, N., additional, Vajkoczy, P., additional, Woitzik, J., additional, Hackbusch, D., additional, Gatzke, N., additional, Duelsner, A., additional, Tsuprykov, O., additional, Slavic, S., additional, Buschmann, I., additional, Kappert, K., additional, Massaro, M., additional, Scoditti, E., additional, Carluccio, M., additional, Storelli, C., additional, Distante, A., additional, De Caterina, R., additional, Barandi, L., additional, Harmati, G., additional, Simko, J., additional, Horvath, B., additional, Szentandrassy, N., additional, Banyasz, T., additional, Magyar, J., additional, Nanasi, P., additional, Kaya, A., additional, Uzunhasan, I., additional, Yildiz, A., additional, Yigit, Z., additional, Turkoglu, C., additional, Doisne, N., additional, Zannad, N., additional, Hivert, B., additional, Cosnay, P., additional, Maupoil, V., additional, Findlay, I., additional, Virag, L., additional, Kristof, A., additional, Koncz, I., additional, Szel, T., additional, Jost, N., additional, Biliczki, P., additional, Papp, J., additional, Varro, A., additional, Bukowska, A., additional, Skopp, K., additional, Hammwoehner, M., additional, Huth, C., additional, Bode-Boeger, S., additional, Goette, A., additional, Workman, A., additional, Dempster, J., additional, Marshall, G., additional, Rankin, A., additional, Revnic, C., additional, Ginghina, C., additional, Revnic, F., additional, Yakushev, S., additional, Petrushanko, I., additional, Makhro, A., additional, Segato Komniski, M., additional, Mitkevich, V., additional, Makarov, A., additional, Gassmann, M., additional, Bogdanova, A., additional, Rutkovskiy, A., additional, Mariero, L., additional, Stenslokken, K., additional, Valen, G., additional, Vaage, J., additional, Dizayee, S., additional, Kaestner, S., additional, Kuck, F., additional, Piekorz, R., additional, Hein, P., additional, Matthes, J., additional, Nurnberg, B., additional, Herzig, S., additional, Hertel, F., additional, Switalski, A., additional, Bender, K., additional, Kienitz, M.-C., additional, Pott, L., additional, Fornai, L., additional, Angelini, A., additional, Erika Amstalden Van Hove, E., additional, Fedrigo, M., additional, Heeren, R., additional, Kruse, M., additional, Pongs, O., additional, Lehmann, H., additional, Martens-Lobenhoffer, J., additional, Roehl, F., additional, Radicke, S., additional, Cotella, C., additional, Sblattero, D., additional, Schaefer, M., additional, Wettwer, E., additional, Santoro, C., additional, Seyler, C., additional, Kulzer, M., additional, Zitron, E., additional, Scholz, E., additional, Welke, F., additional, Thomas, D., additional, Karle, C., additional, Schmidt, K., additional, Dobrev, D., additional, Houshmand, N., additional, Menesi, D., additional, Cotella, D., additional, Szuts, V., additional, Puskas, L., additional, Kiss, I., additional, Deak, F., additional, Tereshchenko, S., additional, Gladyshev, M., additional, Kalachova, G., additional, Syshchik, N., additional, Gogolashvili, N., additional, Dedok, E., additional, Evert, L., additional, Wenzel, J., additional, Brandenburger, M., additional, Bogdan, R., additional, Richardt, D., additional, Reppel, M., additional, Hescheler, J., additional, Dendorfer, A., additional, Terlau, H., additional, Wiegerinck, R., additional, Galvez-Monton, C., additional, Jorge, E., additional, Martinez, R., additional, Ricart, E., additional, Cinca, J., additional, Bagavananthem Andavan, G., additional, Lemmens Gruber, R., additional, Brack, K., additional, Coote, J., additional, Ng, G., additional, Daimi, H., additional, Haj Khelil, A., additional, Neji, A., additional, Ben Hamda, K., additional, Maaoui, S., additional, Aranega, A., additional, Chibani, J., 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Published
2010
Full Text
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6. Plumericin inhibits proliferation of vascular smooth muscle cells by blocking STAT3 signaling via S-glutathionylation.

Author

Heiss EH, Liu R, Waltenberger B, Khan S, Schachner D, Kollmann P, Zimmermann K, Cabaravdic M, Uhrin P, Stuppner H, Breuss JM, Atanasov AG, and Dirsch VM

Subjects
Animals, Apocynaceae chemistry, Cells, Cultured, Cyclin D1 biosynthesis, Indenes chemistry, Iridoids chemistry, Muscle, Smooth, Vascular pathology, Myocytes, Smooth Muscle pathology, Rats, G1 Phase drug effects, Glutathione metabolism, Indenes pharmacology, Iridoids pharmacology, Muscle, Smooth, Vascular metabolism, Myocytes, Smooth Muscle metabolism, Protein Processing, Post-Translational drug effects, Resting Phase, Cell Cycle drug effects, STAT3 Transcription Factor metabolism, Signal Transduction drug effects
Abstract

The etiology of atherosclerosis and restenosis involves aberrant inflammation and proliferation, rendering compounds with both anti-inflammatory and anti-mitogenic properties as promising candidates for combatting vascular diseases. A recent study identified the iridoid plumericin as a new scaffold inhibitor of the pro-inflammatory NF-κB pathway in endothelial cells. We here examined the impact of plumericin on the proliferation of primary vascular smooth muscle cells (VSMC). Plumericin inhibited serum-stimulated proliferation of rat VSMC. It arrested VSMC in the G1/G0-phase of the cell cycle accompanied by abrogated cyclin D1 expression and hindered Ser 807/811-phosphorylation of retinoblastoma protein. Transient depletion of glutathione by the electrophilic plumericin led to S-glutathionylation as well as hampered Tyr705-phosphorylation and activation of the transcription factor signal transducer and activator of transcription 3 (Stat3). Exogenous addition of glutathione markedly prevented this inhibitory effect of plumericin on Stat3. It also overcame downregulation of cyclin D1 expression and the reduction of biomass increase upon serum exposure. This study revealed an anti-proliferative property of plumericin towards VSMC which depends on plumericin's thiol reactivity and S-glutathionylation of Stat3. Hence, plumericin, by targeting at least two culprits of vascular dysfunction -inflammation and smooth muscle cell proliferation -might become a promising electrophilic lead compound for vascular disease therapy.

Published
2016
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7. The interferon stimulated gene 12 inactivates vasculoprotective functions of NR4A nuclear receptors.

Author

Papac-Milicevic N, Breuss JM, Zaujec J, Ryban L, Plyushch T, Wagner GA, Fenzl S, Dremsek P, Cabaravdic M, Steiner M, Glass CK, Binder CJ, Uhrin P, and Binder BR

Subjects
Active Transport, Cell Nucleus, Animals, Carotid Artery Injuries genetics, Carotid Artery Injuries immunology, Carotid Artery Injuries metabolism, Carotid Artery Injuries pathology, Cells, Cultured, Disease Models, Animal, Endothelial Cells metabolism, Endothelial Cells pathology, Feedback, Physiological, Femoral Artery injuries, Femoral Artery pathology, Gene Expression Regulation, Inflammation genetics, Inflammation immunology, Inflammation metabolism, Inflammation pathology, Interferons metabolism, Karyopherins metabolism, Membrane Proteins genetics, Mice, Mice, 129 Strain, Mice, Inbred C57BL, Mice, Knockout, Muscle, Smooth, Vascular injuries, Muscle, Smooth, Vascular metabolism, Muscle, Smooth, Vascular pathology, Myocytes, Smooth Muscle metabolism, Myocytes, Smooth Muscle pathology, Nuclear Receptor Subfamily 4, Group A, Member 1 genetics, Protein Interaction Domains and Motifs, Proteins genetics, RNA Interference, Receptors, Cytoplasmic and Nuclear metabolism, Time Factors, Transcription, Genetic, Transfection, Vascular System Injuries genetics, Vascular System Injuries immunology, Vascular System Injuries metabolism, Vascular System Injuries pathology, Exportin 1 Protein, Carotid Artery Injuries prevention & control, Femoral Artery metabolism, Inflammation prevention & control, Membrane Proteins metabolism, Nuclear Receptor Subfamily 4, Group A, Member 1 metabolism, Proteins metabolism, Vascular System Injuries prevention & control
Abstract

Rationale: Innate and adaptive immune responses alter numerous homeostatic processes that are controlled by nuclear hormone receptors. NR4A1 is a nuclear receptor that is induced in vascular pathologies, where it mediates protection., Objective: The underlying mechanisms that regulate the activity of NR4A1 during vascular injury are not clear. We therefore searched for modulators of NR4A1 function that are present during vascular inflammation., Methods and Results: We report that the protein encoded by interferon stimulated gene 12 (ISG12), is a novel interaction partner of NR4A1 that inhibits the transcriptional activities of NR4A1 by mediating its Crm1-dependent nuclear export. Using 2 models of vascular injury, we show that ISG12-deficient mice are protected from neointima formation. This effect is dependent on the presence of NR4A1, as mice deficient for both ISG12 and NR4A1 exhibit neointima formation similar to wild-type mice., Conclusions: These findings identify a previously unrecognized feedback loop activated by interferons that inhibits the vasculoprotective functions of NR4A nuclear receptors, providing a potential new therapeutic target for interferon-driven pathologies.

Published
2012
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8. Indirubin-3'-monoxime blocks vascular smooth muscle cell proliferation by inhibition of signal transducer and activator of transcription 3 signaling and reduces neointima formation in vivo.

Author

Schwaiberger AV, Heiss EH, Cabaravdic M, Oberan T, Zaujec J, Schachner D, Uhrin P, Atanasov AG, Breuss JM, Binder BR, and Dirsch VM

Subjects
Animals, Arterial Occlusive Diseases metabolism, Arterial Occlusive Diseases pathology, Becaplermin, Cell Cycle drug effects, Cells, Cultured, Constriction, Pathologic, Disease Models, Animal, Dose-Response Relationship, Drug, Endothelial Cells drug effects, Endothelial Cells metabolism, Femoral Artery drug effects, Femoral Artery metabolism, Femoral Artery pathology, Flow Cytometry, Humans, Hyperplasia, Interferon-gamma metabolism, Ki-67 Antigen metabolism, Male, Mice, Mice, Inbred C57BL, Mitogen-Activated Protein Kinases metabolism, Muscle, Smooth, Vascular metabolism, Muscle, Smooth, Vascular pathology, Myocytes, Smooth Muscle metabolism, Myocytes, Smooth Muscle pathology, Phosphorylation, Platelet-Derived Growth Factor metabolism, Proto-Oncogene Proteins c-akt metabolism, Proto-Oncogene Proteins c-sis, Rats, Rats, Sprague-Dawley, STAT3 Transcription Factor genetics, STAT3 Transcription Factor metabolism, Thrombin metabolism, Time Factors, Transfection, Arterial Occlusive Diseases prevention & control, Cell Proliferation, Indoles pharmacology, Muscle, Smooth, Vascular drug effects, Myocytes, Smooth Muscle drug effects, Oximes pharmacology, STAT3 Transcription Factor antagonists & inhibitors, Signal Transduction drug effects
Abstract

Objective: Our goal was to examine the influence of indirubin-3'-monoxime (I3MO), a natural product-derived cyclin-dependent kinase inhibitor, on vascular smooth muscle cell (VSMC) proliferation in vitro, experimentally induced neointima formation in vivo, and related cell signaling pathways., Methods and Results: I3MO dose-dependently inhibited platelet-derived growth factor (PDGF)-BB-induced VSMC proliferation by arresting cells in the G(0)/G(1) phase of the cell cycle as assessed by 5-bromo-2'-deoxyuridine incorporation and flow cytometry. PDGF-induced activation of the kinases Akt, Erk1/2, and p38(MAPK) was not affected. In contrast, I3MO specifically blocked PDGF-, interferon-γ-, and thrombin-induced phosphorylation of signal transducer and activator of transcription 3 (STAT3). Human endothelial cells (EA.hy926) responded to I3MO with increased endothelial nitric oxide synthase activity as assessed via [(14)C]l-arginine/[(14)C]l-citrulline conversion. The specific STAT3 inhibitor Stattic led to decreased VSMC proliferation, and transient expression of a constitutively active form of STAT3 overcame the I3MO-induced cell cycle arrest in mouse embryonic fibroblasts. In a murine femoral artery cuff model, I3MO prevented neointima formation while reducing STAT3 phosphorylation and the amount of proliferating Ki67-positive cells., Conclusions: I3MO represses PDGF- and thrombin-induced VSMC proliferation and, in vivo, neointima formation, likely because it specifically blocks STAT3 signaling. This profile and its positive effect on endothelial NO production turns I3MO into a promising lead compound to prevent restenosis.

Published
2010
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9. Induction of chromosome aberrations in the Allium cepa test system caused by the exposure of cells to benzo(a) pyrene.

Author

Cabaravdic M

Subjects
Mitosis drug effects, Benzo(a)pyrene toxicity, Chromosome Aberrations drug effects, Mutagenicity Tests, Onions genetics
Abstract

Higher plants have been proposed as test organisms for the detection of genotoxic substances in the environment. Several plant test systems are already in use and are found to be as sensitive and reliable as other short-term tests. Allium cepa is one of these plants, which has been used in different studies to detect chromosome aberrations induced by chemicals. The use of non-animal test methods, including in vitro studies, provides importent tools to enhance our understanding of hazardous effect of chemicals, and for predicting these effects in humans. In vitro systems are used principally for screening purposes, and for generating toxicological profiles. Numerous chemicals can generate the breakage or interchange of DNA segments between chromosomal structures. Allium test is used as a screening method for genotoxicity evaluation of different chemical substances, including polycyclic aromatic hydrocarbons (PAHs). Benzo(a)pyrene (BaP), as representative member of PAHs, were investigated of genotoxicity by using Allium roote chromosomes assay. The treatment with different series of concentrations of BaP, ranging from 1.0-50.0 microg/ml respectively. Used BaP caused decreased in the Mitotic index (MI) and increase frequency of abnormal mitosis when compared with the control.

Published
2010

10. Occupational exposure of workers at gas station to inorganic lead.

Author

Cabaravdic M, Mijanovic M, Kusturica J, and Cabaravdic A

Subjects
Adult, Aminolevulinic Acid urine, Blood Cell Count, Humans, Male, Middle Aged, Young Adult, Gasoline, Lead adverse effects, Lead blood, Occupational Exposure
Abstract

Exposure to the lead is public health problem and threat to environment with proven harmful impact on human, including industrial workers and general population. Harmful impacts of exposition to nervous, endocrine, hematological, cardiovascular, immune and reproductive system to the lead are well known. This article addresses the results of retrospective research carried out with attendants at gas station and those who are professionally exposed to inorganic lead (n=73; n=81), during the course of two periodic reviews performed in 2003 and 2008. All subjects underwent physical examination, ECG, were measured blood pressure and laboratory tests encompassing basic hematological parameters, including measuring of blood lead level (BLL), as bioindicators of exposure and biomarkers of toxic impact of the lead, by the means of determining concentration of 6-aminolevulinic acid in urine (ALA).Valued obtained included (arithmetic mean +/- standard deviation): for BLL 42.5 +/- 26.2 microg/L(-1), for ALA 35.2 +/- 10.6 micromol/L(-1). Quoted values are within normal values for general population. Correlation test established positive correlation between BLL and hematological parameters, number of erythrocytes, concentration of hemoglobin and MCV, and the same correlation ratio was established between BLL and years of age, years of service and exposition years of service as well as BLL and GGT. There was not established correlation between ALA and observed hematological parameters, BLL and systole pressure. Data from our research indicate unification between professional exposure to lead and duration of exposure and increase of concentration of BLL, which are far bellow marginalvalue, but do exceed average values of BLL for people of industrial countries with possible generation of harmful impact of lead. Likewise, the results suggest the increase of overall lead load in the body does not have to be necessarily only the result of professional exposure, but of the intake through other channels as well.

Published
2010

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