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    Endothelin Receptor-Independent Correlation Between HSP47 and Collagen in Rabbit Model of Early Atherosclerosis
    (Ortadogu Ad Pres & Publ Co, 2011) Reel, Buket; Cavdar, Zahide; Ergur, Bekir Ugur; Ozkal, Sermin; Ozsarlak-Sozer, Gonen; Oktay, Gulgun; Kerry, Zeliha
    Objective: Collagen in the extracellular matrix (ECM) plays an important role in modulation of response to the vascular injury during the progression of atherosclerosis and restenosis. Collagen can regulate smooth muscle cell (SMC) proliferation, migration and matrix metalloproteinase (MMP) production. Therefore, collagen turnover in the arteries is an important determinant of intimal thickening. Heat shock protein 47 (HSP47), a collagen-specific molecular chaperone, is thought to be essential for the processing and secretion of procollagen molecules. Endothelin (ET) is a strong chemoatractant and mitogen promoting SMC proliferation and migration. The aim of this study was to investigate the possible role of HSP47 and its relation to collagen synthesis, and the effects of a nonselective ETA/ETB receptor antagonist, TAK-044 in collar-induced early atherosclerosis model. Material and Methods: New Zealand white rabbits were divided into two groups. Both groups received vehicle (0.9% NaCl 0.8 ml/kg/day, s.c.) or TAK-044 (5 mg/kg/day, s.c.) for three weeks. On 8th day, a non-occlusive silicon collar was placed around the left carotid artery. The right carotid artery was sham-operated. HSP47 expression in carotid arteries were determined immunohistochemically. Furthermore, total collagen levels, collagen expression and type I procollagen expression were established. Results: HSP47 expression correlated with collagen expression did not change in collared arteries. TAK-044 treatment did not affect HSP47 and collagen levels. Conclusion: There was a correlation between HSP47 expression and collagen expression in carotid arteries. However, intimal thickening did not induce HSP47 expression and early collagen development. The ineffectivenes of TAK-044 suggests that ET-1 signaling may not be implicated in HSP47 and collagen in this model.
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    Glutathione Depletion by Buthionine Sulfoximine Induces Oxidative Damage to DNA in Organs of Rabbits in Vivo
    (Amer Chemical Soc, 2009) Gokce, Goksel; Ozsarlak-Sozer, Gonen; Oktay, Gulgun; Kirkali, Gueldal; Jaruga, Pawel; Dizdaroglu, Miral; Kerry, Zeliha
    Glutathione (GSH) exists in mammalian tissues in vivo at high concentrations and plays an important protective role against oxidatively induced damage to biological molecules, including DNA. We investigated oxidatively Induced damage to DNA by GSH depletion in different organs of rabbits in vivo. Rabbits were treated subcutaneously with buthionine sulfoximine (BSO), an effective GSH-depleting compound. GSH levels were measured in heart, brain, liver, and kidney of animals. BSO treatment significantly reduced GSH levels in heart, brain, and liver, but not in kidney. DNA was isolated from these tissues to test whether GSH depletion causes oxidatively induced DNA damage in vivo. Gas chromatography-mass spectrometry and liquid chromatography-mass spectrometry with isotope dilution methods were applied to measure typical products of oxidatively induced damage in isolated DNA samples. Several such products were identified and quantified in all organs. BSO treatment caused significant formation of 8-hydroxyguanine, 2,6-diamino-4-hydroxy-5-formamidopyrimidine, 8-hydroxyadenine, and (5'S)-8,5'-cyclo-2'-deoxyadenosine in DNA of organs of rabbits. Animals were fed with the semiessential amino acid 2-aminoethanesulfonic acid (taurine) during BSO treatment. Taurine significantly inhibited GSH depletion and also formation of DNA products. Depletion of GSH correlated well with formation of DNA products, indicating the role of GSH in preventing oxidatively induced DNA damage. Our findings might contribute to the understanding of pathologies associated with DNA damage, oxidative stress, and/or defective antioxidant responses and improve our understanding of the effect of BSO in increasing the efficacy of anticancer therapeutics.
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    MMP-2 and MMP-9 Alteration in Response to Collaring in Rabbits: The Effects of Endothelin Receptor Antagonism
    (Sage Publications Inc, 2009) Reel, Buket; Oktay, Gulgun; Ozkal, Sermin; Islekel, Huray; Ozer, Erdener; Ozsarlak-Sozer, Gonen; Cavdar, Zahide; Akhisaroglu, Serpil Tanriverdi; Kerry, Zeliha
    Matrix metalloproteinases (MMPs), and, in particular, gelatinases (MMP-2 and MMP-9), have been implicated in vascular cell proliferation and/or migration, contributing to intimal thickening, an essential stage in the development of atherosclerosis and restenosis following balloon angioplasty. Endothelin, a strong chemoatractant and mitogen, has been shown to promote smooth muscle cell proliferation and migration by activating MMPs via endothelin-A (ETA) receptors. The positioning of a soft silicon collar around the left carotid artery in rabbits results in intimal thickening. In this study, we investigate the possible role of gelatinases and the effect of a nonselective ETA/ETB receptor antagonist, TAK-044 (5 mg/kg body weight/day, subcutaneously [sc]), on these enzymes. Our results demonstrated that both MMP-2 and MMP-9 activities increased in response to collaring in placebo group, while treatment with TAK-044 significantly suppressed both gelatinase activities and proMMP-2 levels, and inhibited intimal thickening in collared arteries. These results suggest that either enhanced MMP expression or endothelin receptor antagonism may be involved in the formation of intimal thickening in this model.
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    MMP-2 and MMP-9 Alteration in Response to Collaring in Rabbits: The Effects of Endothelin Receptor Antagonism
    (Sage Publications Inc, 2009) Reel, Buket; Oktay, Gulgun; Ozkal, Sermin; Islekel, Huray; Ozer, Erdener; Ozsarlak-Sozer, Gonen; Cavdar, Zahide; Akhisaroglu, Serpil Tanriverdi; Kerry, Zeliha
    Matrix metalloproteinases (MMPs), and, in particular, gelatinases (MMP-2 and MMP-9), have been implicated in vascular cell proliferation and/or migration, contributing to intimal thickening, an essential stage in the development of atherosclerosis and restenosis following balloon angioplasty. Endothelin, a strong chemoatractant and mitogen, has been shown to promote smooth muscle cell proliferation and migration by activating MMPs via endothelin-A (ETA) receptors. The positioning of a soft silicon collar around the left carotid artery in rabbits results in intimal thickening. In this study, we investigate the possible role of gelatinases and the effect of a nonselective ETA/ETB receptor antagonist, TAK-044 (5 mg/kg body weight/day, subcutaneously [sc]), on these enzymes. Our results demonstrated that both MMP-2 and MMP-9 activities increased in response to collaring in placebo group, while treatment with TAK-044 significantly suppressed both gelatinase activities and proMMP-2 levels, and inhibited intimal thickening in collared arteries. These results suggest that either enhanced MMP expression or endothelin receptor antagonism may be involved in the formation of intimal thickening in this model.
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    The report of the 1st Turkey in vitro diagnostic symposium results
    (Walter De Gruyter Gmbh, 2017) Kocdor, Hilal; Sezer, Ebru; Erbayraktar, Zubeyde; Pabuccuoglu, Aysun; Onat, Taner; Oktay, Gulgun; Guner, Gul; Yener, Nilgun; Sagin, Ferhan; Aslan, Diler
    The 1st Turkish in vitro Diagnostic Symposium was organized in Izmir between the dates 18-20 February 2016 with cooperation of Turkish Biochemistry Society Izmir Branch and Dokuz Eylul University Institute of Health Sciences. This article presents a collection of the subjects, recommendations and results included in the final report of the symposium. Symposium subjects were analysed under separate titles and evaluated together with results obtained from various reports on medical devices (MD) in the last decade. According to the final report, the subjects to be considered on preferential basis include "configuration of the websites of legal authorities, standardization and accreditation institutions in a way to access work on in vitro Diagnostic (IVD)", "activation of university-industry cooperation", "determination of national standards parallel to international standards" and " carrying out the statistics about IVD-MD in Turkey as immediate as possible". Drawing attention to the fact that there is a requirement for competent man power for every-stage of IVD-MD lifecycle, it is recommended that postgraduate education programmes are founded to serve these fields. Consequently, this symposium enabled to determine the basic problems about the sector by bringing together the stakeholders related to IVDMD field and to come up with an action plan in accordance with the recommendations.
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    Taurine inhibits increased MMP-2 expression in a model of oxidative stress induced by glutathione depletion in rabbit heart
    (Elsevier Science Bv, 2013) Sevin, Gulnur; Ozsarlak-Sozer, Gonen; Keles, Didem; Gokce, Goksel; Reel, Buket; Ozgur, Halil Hakan; Oktay, Gulgun; Kerry, Zeliha
    Matrix metalloproteinase enzymes (MMPs) activated by oxidative stress are involved in the pathogenesis of cardiovascular diseases. Glutathione (GSH) plays an important protective role against oxidatively induced damage in mammalian tissues. We investigated the possible role of gelatinases and the effect of the semiessential amino acid 2-aminoethanesulfonic acid (taurine) in oxidatively induced damage by GSH depletion in rabbit cardiac tissues. Rabbits were treated with buthionine sulfoximine (BSO), an effective GSH-depleting compound. BSO treatment significantly reduced GSH and increased MDA (malondialdehyde) levels. BSO treatment caused significant increase in proMMP-2 levels. MMP-9 (pro and active) expressions were not found in either treated- or untreated heart tissues. TIMP-1(endogenous inhibitor of MMP-9) and MT-MMP1 (endogenous activator of MMP-2) were not affected by BSO. Immunoscoring showed that MMP-2 expression significantly increased in hearts from BSO treated group but MMP-9 antibody did not show any significant positive immunostaining from all groups. Type I procollagen and total collagen did not significantly alter in heart tissues from all treatment groups. Taurine restored the increased MDA and the diminished GSH levels by BSO treatment. Pro MMP-2 expression was prevented by taurine. These results suggest that MMP-2 is a major gelanitase in rabbit hearts under oxidative stress and pharmacological inhibition of MMP-2 activation by taurine could represent a useful strategy for the prevention and/or treatment of different cardiovascular disorders. (C) 2013 Elsevier B.V. All rights reserved.