Araştırma Çıktıları

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Author: search.filters.author.Baykal, Ahmet TarikHas files: No

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    Tumor necrosis factor-alpha induced caspase-3 activation-related iNOS gene expression in ADP-activated platelets
    (TUBITAK SCIENTIFIC \& TECHNICAL RESEARCH COUNCIL TURKEY, 2017-01-01) Cevik, Ozge; Adiguzel, Zelal; Baykal, Ahmet Tarik; Sener, Azize
    Platelets are sensitive cells and are easily activated by different stimulants in the circulation system. It is known that tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine and plays a role in inflammation. The role of TNF-a in the apoptotic process in blood platelets is unknown. In order to study the formation of apoptosis in platelets after incubation with TNF-alpha and/or ADP, several biomarkers were chosen: phosphatidylserine (PS) exposure and P-selectin binding
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    Neonatal Neurodegeneration in Alzheimer's Disease Transgenic Mouse Model
    (IOS PRESS, 2018-01-01) Mazi, Aise Rumeysa; Arzuman, Aysegul Sumeyye; Gurel, Busra; Sahin, Betul; Tuzuner, Mete Bora; Ozansoy, Mehmet; Baykal, Ahmet Tarik
    Alzheimer's disease (AD) is a progressive disorder characterized by a variety of molecular pathologies causing cortical dementia with a prominent memory deficit. Formation of the pathology, which begins decades before the diagnosis of the disease, is highly correlated with the clinical symptoms. Several proteomics studies were performed using animal models to monitor the alterations of the brain tissue proteome at different stages of AD. However, proteome changes in the brain regions of newborn transgenic mouse model have not been investigated yet. To this end, we analyzed protein expression alterations in cortex, hippocampus and cerebellum of transgenic mice carrying five familial AD mutations (5XFAD) at neonatal day-1. Our results indicate a remarkable difference in protein expression profile of newborn 5XFAD brain with region specific variations. Additionally, the proteins, which show similar expression alteration pattern in postmortem human AD brains, were determined. Bioinformatics analysis showed that the molecular alterations were mostly related to the cell morphology, cellular assembly and organization, and neuroinflammation. Moreover, morphological analysis revealed that there is an increase in neurite number of 5XFAD mouse neurons in vitro. We suggest that, molecular alterations in the AD brain exist even at birth, and perhaps the disease is silenced until older ages when the brain becomes vulnerable.
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    Proteomic profiling of HBV infected liver biopsies with different fibrotic stages
    (BMC, 2017-01-01) Katrinli, Seyma; Ozdil, Kamil; Sahin, Abdurrahman; Ozturk, Oguzhan; Kir, Gozde; Baykal, Ahmet Tarik; Akgun, Emel; Sarac, Omer Sinan; Sokmen, Mehmet; Doganay, H. Levent; Doganay, Gizem Dinler
    Background: Hepatitis B virus (HBV) is a global health problem, and infected patients if left untreated may develop cirrhosis and eventually hepatocellular carcinoma. This study aims to enlighten pathways associated with HBV related liver fibrosis for delineation of potential new therapeutic targets and biomarkers. Methods: Tissue samples from 47 HBV infected patients with different fibrotic stages (F1 to F6) were enrolled for 2D-DIGE proteomic screening. Differentially expressed proteins were identified by mass spectrometry and verified by western blotting. Functional proteomic associations were analyzed by EnrichNet application. Results: Fibrotic stage variations were observed for apolipoprotein A1 (APOA1), pyruvate kinase PKM (KPYM), glyceraldehyde 3-phospahate dehydrogenase (GAPDH), glutamate dehydrogenase (DHE3), aldehyde dehydrogenase (ALDH2), alcohol dehydrogenase (ALDH1A1), transferrin (TRFE), peroxiredoxin 3 (PRDX3), phenazine biosynthesis-like domain-containing protein (PBLD), immuglobulin kappa chain C region (IGKC), annexin A4 (ANXA4), keratin 5 (KRT5). Enrichment analysis with Reactome and Kegg databases highlighted the possible involvement of platelet release, glycolysis and HDL mediated lipid transport pathways. Moreover, string analysis revealed that HIF-1 alpha (Hypoxia-inducible factor 1-alpha), one of the interacting partners of HBx (Hepatitis B X protein), may play a role in the altered glycolytic response and oxidative stress observed in liver fibrosis. Conclusions: To our knowledge, this is the first protomic research that studies HBV infected fibrotic human liver tissues to investigate alterations in protein levels and affected pathways among different fibrotic stages. Observed changes in the glycolytic pathway caused by HBx presence and therefore its interactions with HIF-1a can be a target pathway for novel therapeutic purposes.
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    Brain region-specific amyloid plaque-associated myelin lipid loss, APOE deposition and disruption of the myelin sheath in familial Alzheimer's disease mice
    (WILEY, 2020-01-01) Kaya, Ibrahim; Jennische, Eva; Lange, Stefan; Baykal, Ahmet Tarik; Malmberg, Per; Fletcher, John S.
    There is emerging evidence that amyloid beta (A beta) aggregates forming neuritic plaques lead to impairment of the lipid-rich myelin sheath and glia. In this study, we examined focal myelin lipid alterations and the disruption of the myelin sheath associated with amyloid plaques in a widely used familial Alzheimer's disease (AD) mouse model
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    Proteomics analysis of mitochondrial dysfunction triggered by complex specific electron transport chain inhibitors reveals common pathways involving protein misfolding in an SH-SY5Y in vitro cell model
    (TUBITAK SCIENTIFIC \& TECHNICAL RESEARCH COUNCIL TURKEY, 2017-01-01) Sahin, Betul; Baykal, Ahmet Tarik
    Mitochondrial dysfunction has been previously identified in neurodegenerative diseases such as Alzheimer disease, Huntington disease, and Parkinson disease. Chemical inhibition of the mitochondrial electron transport chain (ETC) was shown to trigger symptoms in animal models similar to those observed in human neurodegenerative diseases. In order to understand the effect of mitochondrial dysfunction on the proteome level, LC-MSE-based bottom-up, label-free differential proteomics expression analysis was used to monitor protein level changes in SH-SY5Y neuroblastoma cells induced by ETC-specific inhibitors (MPTP, 3-NP, sodium azide, antimycin A, and oligomycin). A total of 379 proteins were identified across the sample set and 75 of them were found to be differentially expressed (>30\% fold change). Complex-specific inhibition of the five ETS complexes were expected to result in the aberrant regulation of different molecular pathways, but the bioinformatics analysis of the LC-MSMS data showed that the differentially expressed proteins were mostly involved in similar metabolic processes. The findings suggest that the complex-specific alterations may not be directly linked to neurodegenerative pathways, but could be considered contributors. Moreover, the proteins that showed the highest protein expression difference (>60\% fold change) are involved in pathways regarding protein-folding and response to unfolded proteins. The results indicate that protein misfolding pathways might have a central role in the genesis and progression of neurodegenerative diseases and that label-free LC-MSMS proteomics analysis is an invaluable approach for studying of molecular pathways in neurodegeneration.
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    Transcriptomics and Proteomics Analyses Reveal JAK Signaling and Inflammatory Phenotypes during Cellular Senescence in Blind Mole Rats: The Reflections of Superior Biology
    (MDPI, 2022-01-01) Inci, Nurcan; Akyildiz, Erdogan Oguzhan; Bulbul, Abdullah Alper; Turanli, Eda Tahir; Akgun, Emel; Baykal, Ahmet Tarik; Colak, Faruk; Bozaykut, Perinur
    The blind mole rat (BMR), a long-living subterranean rodent, is an exceptional model for both aging and cancer research since they do not display age-related phenotypes or tumor formation. The Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling is a cytokine-stimulated pathway that has a crucial role in immune regulation, proliferation, and cytokine production. Therefore, the pathway has recently attracted interest in cellular senescence studies. Here, by using publicly available data, we report that JAK-STAT signaling was suppressed in the BMR in comparison to the mouse. Interestingly, our experimental results showed upregulated Jak1/2 expressions in BMR fibroblasts during the replicative senescence process. The transcriptomic analysis using publicly available data also demonstrated that various cytokines related to JAK-STAT signaling were upregulated in the late passage cells, while some other cytokines such as MMPs and SERPINs were downregulated, representing a possible balance of senescence-associated secretory phenotypes (SASPs) in the BMR. Finally, our proteomics data also confirmed cytokine-mediated signaling activation in senescent BMR fibroblasts. Together, our findings suggest the critical role of JAK-STAT and cytokine-mediated signaling pathways during cellular senescence, pointing to the possible contribution of divergent inflammatory factors to the superior resistance of aging and cancer in BMRs.