Person: YILMAZ, BETÜL
Loading...
Email Address
Birth Date
Research Projects
Organizational Units
Job Title
Last Name
YILMAZ
First Name
BETÜL
Name
6 results
Search Results
Now showing 1 - 6 of 6
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 Metadata only High cholesterol diet-mediated unfolded protein response activation enhances autophagic cell death in heart tissue(ELSEVIER SCIENCE INC, 2017) YILMAZ, BETÜL; Sozen, Erdi; Yazgan, Burak; Tok, Olgu Enis; Ercan, Feriha; Karademir, Betul; Ozer, Nesrin KartalPublication Metadata only Lipid rafts and redox regulation of cellular signaling in cholesterol induced atherosclerosis(2010) YILMAZ, BETÜL; Catalgol B., Ozer N.K.Redox mediated signaling mechanisms play crucial roles in the pathogenesis of several cardiovascular diseases. Atherosclerosis is one of the most important disorders induced mainly by hypercholesterolemia. Oxidation products and related signaling mechanisms are found within the characteristic biomarkers of atherosclerosis. Several studies have shown that redox signaling via lipid rafts play a significant role in the regulation of pathogenesis of many diseases including atherosclerosis. This review attempts to summarize redox signaling and lipid rafts in hypercholesterolemia induced atherosclerosis. © 2010 Bentham Science Publishers Ltd.Publication Metadata only Effects of vitamin E on peroxisome proliferator-activated receptor gamma and nuclear factor-erythroid 2-related factor 2 in hypercholesterolemia-induced atherosclerosis(ELSEVIER SCIENCE INC, 2014) SÖZEN, AHMET ERDİ; Bozaykut, Perinur; Karademir, Betul; Yazgan, Burak; Sozen, Erdi; Siow, Richard C. M.; Mann, Giovanni E.; Ozer, Nesrin KartalAtherosclerosis and associated cardiovascular complications such as stroke and myocardial infarction are major causes of morbidity and mortality. We have previously reported a significant increase in mRNA levels of the scavenger receptor CD36 in aortae of cholesterol-fed rabbits and shown that vitamin E treatment attenuated increased CD36 mRNA expression. In the present study, we further investigated the redox signaling pathways associated with protection against atherogenesis induced by high dietary cholesterol and correlated these with CD36 expression and the effects of vitamin E supplementation in a rabbit model. Male albino rabbits were assigned to either a control group fed with a low vitamin E diet alone or a test group fed with a low vitamin E diet containing 2% cholesterol in the absence or presence of daily intramuscular injections of vitamin E (50 mg/kg). To elucidate the mechanisms by which vitamin E supplementation alters the effects of hypercholesterolemia in rabbit aortae, we measured peroxisome proliferator-activated receptor gamma (PPAR gamma), ATP-binding cassette transporter A1 (ABCA1), and matrix metalloproteinase-1 (MMP-1) mRNA levels by quantitative RT-PCR and the expression of MMP-1, nuclear factor-erythroid 2-related factor 2 (Nrf2), and glutathione S-transferase alpha (GST alpha) protein by immunoblotting. The increased MMP-1 and decreased GSTa expression observed suggests that a cholesterol-rich diet contributes to the development of atherosclerosis, whereas vitamin E supplementation affords protection by decreasing MMP-1 and increasing PPAR gamma, GSTa, and ABCA1 levels in aortae of rabbits fed a cholesterol-rich diet. Notably, protein expression of Nrf2, the antioxidant transcription factor, was increased in both the cholesterol-fed and the vitamin E-supplemented groups. Although Nrf2 activation can promote CD36-mediated cholesterol uptake by macrophages, the increased induction of Nrf2-mediated antioxidant genes is likely to contribute to decreased lesion progression. Thus, our study demonstrates that Nrf2 can mediate both pro- and antiatherosclerotic effects. (C) 2014 Elsevier Inc. All rights reserved.Publication Metadata only Endoplasmic reticulum stress related molecular mechanisms in nonalcoholic steatohepatitis(ELSEVIER IRELAND LTD, 2016) ŞAHİN, ALİ; Bozaykut, Perinur; Sahin, Ali; Karademir, Betul; Ozer, Nesrin KartalNonalcoholic steatohepatitis (NASH) is considered to be a common health problem since the incidence of nonalcoholic fatty liver disease (NAFLD) has increased in recent years. Disturbed hepatic cholesterol homeostasis and free cholesterol accumulation in liver results in increased oxidative stress leading to the endoplasmic reticulum (ER) stress. Activated ER stress maintains protein homeostasis however, delayed or inadequate ER stress responses may induce fat accumulation, insulin resistance, inflammation, apoptosis, and autophagy, all of which increase with age and play crucial roles in the pathogenesis of NASH. In aging research, there is a growing interest for the role of ER stress in the progression of NASH since aging seems to favor NAFLD according to its pathogenesis. On the other hand, specific microRNAs (miRNAs) expression profiles are strongly related with ER stress as well as NASH progresses. This review highlights molecular mechanisms related to ER stress in the pathogenesis of NASH and miRNAs for the progression and treatment of the disease. (C) 2016 Elsevier Ireland Ltd. All rights reserved.Publication Metadata only Identification of differentially expressed proteins in atherosclerotic aorta and effect of vitamin E(ELSEVIER, 2013) YILMAZ, BETÜL; Kaga, Elif; Karademir, Betul; Baykal, Ahmet Tarik; Ozer, Nesrin KartalAtherosclerosis is a chronic inflammatory disorder that occurs as a result of mononuclear lymphocyte infiltration to the arterial wall, smooth muscle cell proliferation and damage in the arterial wall caused by extracellular matrix accumulation. Besides several genetic and environmental factors, increased serum cholesterol and oxidized low density lipoproteins are considered to be major inducing factors of atherosclerosis. Several protective agents have been used to prevent the progression of atherosclerosis and recently vitamin E has been focused because of its significant role in signaling mechanisms. Since many different cell types are involved in the development of hypercholesterolemia induced atherosclerosis, it is important to investigate wide range of proteins to highlight the pathologic and diagnostic mechanisms. In this study, by using proteomic technique, we identified differentially expressed proteins following cholesterol and also vitamin E treatments. The expressions of apolipoprotein AI and apolipoprotein E involved in lipid metabolism, peroxiredoxin 1, peroxiredoxin 2 and thioredoxin involved in antioxidant system, 14-3-3 protein zeta delta and 14-3-3 protein beta alpha in cell signaling, biglycan, vimentin, tropomyosin and smooth muscle a-actin as structural and contractile proteins have been discussed. Biological significance We observed several protein alterations in aorta of cholesterol fed and vitamin E treated rabbits. These differentially expressed proteins associated with key mechanisms involved in atherosclerosis and signaling mechanisms related with vitamin E. These findings for different proteins might be helpful for deciphering the pathogenesis in atherosclerosis. In addition it provides a new perspective to understand mechanisms of beneficial effect of vitamin E on the signaling pathways in atherogenesis. (C) 2013 Elsevier B.V. All rights reserved.