Person: YILMAZ, BETÜL
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YILMAZ
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BETÜL
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Publication Open Access Cytotoxicity of Different Nano Composite Resins on Human Gingival and Periodontal Ligament Fibroblast Cell Lines: An In Vitro Study(MDPI, 2020-03-01) YILMAZ GÖLER, AYŞE MİNE; Kavuncu, Gamze; Yilmaz, Ayse Mine; Yilmaz, Betul Karademir; Atali, Pinar Yilmaz; Altunok, Elif Cigdem; Kuru, Leyla; Agrali, Omer BirkanThe aim of this study is to determine the cytotoxicity of three different nano composite resins (CRs) on human gingival fibroblast (hGF) and periodontal ligament fibroblast (hPDLF) cell lines. These CRs selected were nanohybrid organic monomer-based Admira Fusion (AF), nanohybrid Bis-(acryloyloxymethyl) tricyclo [5.2.1.0.sup.2,6] decane-based Charisma Topaz (CT), and supra nano filled resin-based Estelite Quick Sigma (EQS). MTT assay was performed to assess the cytotoxicity of CRs at 24 h and one week. AF and EQS applied on hGF cells at 24 h and one week demonstrated similar cytotoxic outcomes. Cytotoxicity of CT on hGF cells at one week was higher than 24 h (p = 0.04). Cytotoxicity of CT on hGF cells was higher at 24 h (p = 0.002) and one week (p = 0.009) compared to control. All composites showed higher cytotoxicity on hPDLF cells at one week than the 24 h (AF; p = 0.02, CT; p = 0.02, EQS; p = 0.04). AF and EQS demonstrated lower cytotoxicity on hPDLF cells than the control group at 24 h (AF; p = 0.01, EQS; p = 0.001). CT was found more cytotoxic on hPDLF cells than the control (p = 0.01) and EQS group (p = 0.008) at one week. The cytotoxicity of CRs on hGF and hPDLF cells vary, according to the type of composites, cell types, and exposure time.Publication Metadata only Repair of critical size defects using bioactive glass seeded with adipose-derived mesenchymal stem cells(2016-05-25) AKDENİZ DOĞAN, ZEYNEP DENİZ; SAÇAK, BÜLENT; YILMAZ, BETÜL; ERCAN, FERİHA; AKDENİZ DOĞAN Z. D., SAÇAK B., YILMAZ B., ERCAN F., ÇELEBİLER Ö. B.Publication Open Access Molecular cardiotoxic effects of proteasome inhibitors carfilzomib and ixazomib and their combination with dexamethasone involve mitochondrial dysregulation(2023-01-01) YILMAZ, BETÜL; JANNUZZI A. T., Korkmaz N. S., GÜNAYDIN AKYILDIZ A., Arslan Eseryel S., Karademir Yilmaz B., ALPERTUNGA B.With the development and approval of new proteasome inhibitors, proteasome inhibition is increasingly recognized in cancer therapy. Besides successful anti-cancer effects in hematological cancers, side effects such as cardiotoxicity are limiting effective treatment. In this study, we used a cardiomyocyte model to investigate the molecular cardiotoxic mechanisms of carfilzomib (CFZ) and ixazomib (IXZ) alone or in combination with the immunomodulatory drug dexamethasone (DEX) which is frequently used in combination therapies in the clinic. According to our findings, CFZ showed a higher cytotoxic effect at lower concentrations than IXZ. DEX combination attenuated the cytotoxicity for both proteasome inhibitors. All drug treatments caused a marked increase in K48 ubiquitination. Both CFZ and IXZ caused an upregulation in cellular and endoplasmic reticulum stress protein (HSP90, HSP70, GRP94, and GRP78) levels and DEX combination attenuated the increased stress protein levels. Importantly, IXZ and IXZ-DEX treatments caused upregulation of mitochondria fission and fusion gene expression levels higher than caused by CFZ and CFZ-DEX combination. The IXZ-DEX combination reduced the levels of OXPHOS proteins (Complex II–V) more than the CFZ-DEX combination. Reduced mitochondrial membrane potential and ATP production were detected with all drug treatments in cardiomyocytes. Our findings suggest that the cardiotoxic effect of proteasome inhibitors may be due to their class effect and stress response and mitochondrial dysfunction may be involved in the cardiotoxicity process.Publication Metadata only Hypercholesterolemia Mediated Endoplasmic Reticulum Stress Response Might Be Related to Autophagic Death of Cardiomyocytes in Heart Failure(ELSEVIER SCIENCE INC, 2016) YILMAZ, BETÜL; Ozer, Nesrin Kartal; Sozen, A. Erdi; Yazgan, Burak; Karademir, BetulPublication Metadata only Repair of critical size defects using bioactive glass seeded with adipose-derived mesenchymal stem cells(WILEY, 2017) YILMAZ, BETÜL; Sacak, Bulent; Certel, Furkan; Akdeniz, Zeynep D.; Karademir, Betul; Ercan, Feriha; Ozkan, Naziye; Akpinar, Ihsan Nuri; Celebiler, OzhanBioactive glass has been demonstrated as a biocompatible bone substitute. However bone healing process can be prolonged due to late resorption of the material. Adipose derived stem cells (ASC) have osteogenic differentiation potential and hence can be a cell source for bone regeneration. The aim of this study was to test whether combination of bioactive glass with ASCs would enhance bone regeneration. Following creation of critical sized defects on the calvaria of 32 Wistar rats, the animals were randomly divided into four groups: Group C (control): Defects were left untreated; Group G: Defects were covered with autologous bone graft; Group BG: Defects were filled with bioactive glass; Group BG/ASC: Defects were filled with bioactive glass seeded with ASCs. The defect size was significantly greater in Group compared to all other groups. Bone density was significantly lower in Group C compared to Group G and Group BG/ASC. Bone regeneration score of Group C was significantly lower than other groups. Group BG/ASC demonstrated lamellar bone and havers canal formation. The results of this study demonstrated that bioactive glass implanted with ASC is a biocompatible construct stimulating radiologically and histologically evident bone regeneration similar to autologous bone grafting. (C) 2016 Wiley Periodicals, Inc.Publication Metadata only Combination of proteasome inhibitors with temozolomide to increase the anti-tumor effect in 3D culture model of glioblastoma(ELSEVIER SCIENCE INC, 2018) YILMAZ GÖLER, AYŞE MİNE; Unal, Semra; Gokce, Tilbe; Arslan, Sema; Yilmaz, Ayse Mine; Gunduz, Oguzhan; Karademir, BetulPublication Metadata only Cathepsins D and L reduce the toxicity of advanced glycation end products(ELSEVIER SCIENCE INC, 2012) YILMAZ, BETÜL; Grimm, Stefanie; Horlacher, Melanie; Catalgol, Betul; Hoehn, Annika; Reinheckel, Thomas; Grune, TilmanAdvanced glycation end product-modified proteins are known for accumulating during aging and in several pathological conditions such as diabetes, renal failure, and neurodegenerative disorders. There is little information about the intracellular fate of endocytosed advanced glycation end products (AGES) and their influence on proteolytic systems. However, it is known that the lysosomal system is impaired during aging. Therefore, undegraded material may accumulate and play a considerable role in the development of diverse diseases. To investigate if AGEs can be degraded and to test whether they accumulate because of impaired lysosomal proteases we studied the effects of advanced glycation end products on the endosomal lysosomal system. Five different types of AGEs were generated by bovine serum albumin incubation with glyoxal, methylglyoxal, glucose, fructose, and ribose. The first experiments revealed the uptake of AGEs by the macrophage cell line RAW 264.7. Further investigations demonstrated an increase in cathepsin D and L activity and an increase in mature cathepsins D and L Increased activities were accompanied by the presence of more lysosomes, measured by staining with LysoTracker blue. To specify the roles of cathepsins D and L we used knockout cells to test the roles of both cathepsins on the toxicity of advanced glycation end products. In summary we conclude that both cathepsins are required for a reduction in advanced glycation end product-induced cytotoxicity. (C) 2012 Elsevier Inc. All rights reserved.Publication Metadata only ER stress related lipid accumulation and apoptotic cell death in nonalcoholic fatty liver diesease(ELSEVIER SCIENCE INC, 2017) ŞAHİN, ALİ; Demirel, Tugce; Sozen, Erdi; Sahin, Ali; Karademir, Betul; Ozer, Nesrin KartalPublication Open Access Potential role of proteasome on c-jun related signaling in hypercholesterolemia induced atherosclerosis(ELSEVIER SCIENCE BV, 2014) SÖZEN, AHMET ERDİ; Sozen, Erdi; Karademir, Betul; Yazgan, Burak; Bozaykut, Perinur; Ozer, Nesrin KartalAtherosclerosis and its complications are major causes of death all over the world. One of the major risks of atherosclerosis is hypercholesterolemia. During atherosclerosis, oxidized low density lipoprotein (oxLDL) regulates CD36-mediated activation of c-jun amino terminal kinase-1 (JNK1) and modulates matrix metalloproteinase (MMP) induction which stimulates inflammation with an invasion of monocytes. Additionally, inhibition of proteasome leads to an accumulation of c-jun and phosphorylated c-jun and activation of activator protein-1 (AP-1) related increase of MMP expression. We have previously reported a significant increase in cluster of differentiation 36 (CD36) mRNA levels in hypercholesterolemic rabbits and shown that vitamin E treatment prevented the cholesterol induced increase in CD36 mRNA expression. In the present study, our aim is to identify the signaling molecules/transcription factors involved in the progression of atherosclerosis following CD36 activation in an in vivo model of hypercholesterolemic (induced by 2% cholesterol containing diet) rabbits. In this direction, proteasomal activities by fluorometry and c-jun, phospo c-jun, JNK1, MMP-9 expressions by quantitative RT-PCR and immunoblotting were tested in aortic tissues. The effects of vitamin E on these changes were also investigated in this model. As a result, c-jun was phosphorylated following decreased proteasomal degradation in hypercholesterolemic group. MMP-9 expression was also increased in cholesterol group rabbits contributing to the development of atherosclerosis. In addition, vitamin E showed its effect by decreasing MMP-9 levels and phosphorylation of c-jun. (C) 2014 The Authors. Published by Elsevier B.V.Publication Metadata only Redox Regulation and Cancer Therapy(BENTHAM SCIENCE PUBL LTD, 2018) YALÇIN, AHMET SUHA; Yalcin, A. Suha; Karademir, Betul