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    Association among ABCA7 Gene Polymorphism, rs3764650 and Alzheimer's Disease in the Turkish Population
    (Canadian Soc Clinical Investigation, 2015) Oznur, Murat; Hatipoglu, Omer F.; Ayturk, Zubeyde; Dede, Serap; Akbas, Kubra; Aydin, Duygu; Urhan, Ayse
    Purpose: Alzheimer's disease (AD), the most common form of dementia, is an irreversible and progressive neurodegenerative disease that is characterized by the progressive loss of cognitive functions, behavioral and psychological disorders and a decrease in daily routine activities. Among people aged 65 years and over, AD is steadily increasing. Genome-wide association studies have shown that various gene polymorphisms are highly associated with the pathogenesis of AD. Among them, ABCA7 gene polymorphism has been identified as one of the genetic risks. The purpose of this study was to investigate the relationship among ABCA7 gene polymorphism, rs3764650 and AD, and to determine if it could be use as a biomarker for AD susceptibility in the Turkish population. Methods: Peripheral blood samples of 54 Alzheimer's patients and 57 control subjects were collected. Genomic DNA was isolated by SDS/proteinase K treatment followed by phenolchloroform extraction and ethanol precipitation. The presence of the ABCA7 gene rs3764650 polymorphism was investigated by PCR-RFLP and selected samples were confirmed by DNA sequencing. Results: In the Turkish population, the ABCA7 gene rs3764650 polymorphism did not show a significant association with AD when compared with the control group (p>0.05). APOE-epsilon 3 allele frequencies were higher in both AD patients and control subjects (76.85% and 84.21%, respectively). Conclusion: Both previously published studies and our current study did not cover the complete genetic variation in the gene. To detect variants that are disease-related, studies with larger sample sizes are needed.
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    NF-?B and MAPKs are involved in resistin-caused ADAMTS-5 induction in human chondrocytes
    (Canadian Soc Clinical Investigation, 2015) Hatipoglu, Omer F.; Yaykasli, Kursat O.; Dogan, Mustafa; Yaykasli, Emine; Bender, Onur; Yasar, Tugce; Tapan, Safa
    Purpose: Chronic inflammation is an important etiological factor in the development of arthritic diseases. Several factors contribute to aggregation of chronic inflammation, including the presence of excess adipose tissue. Methods: The putative induction mechanisms of ADAMTS-5 by resistin were investigated in normal primary human articular chondrocytes. Expression levels of the ADAMTS-5 gene were determined at several resistin doses and durations. Results: Human chondrocytes were activated and associated with upregulated ADAMTS-5 gene expression after exposure to resistin (also known as adipose tissue-specific secretary factor, ADSF). Release of ADAMTS-5 leads to joint cartilage degradation, a key event in the development of arthritic diseases rheumatoid arthritis (RA) and osteoarthritis (OA). Activation of chondrocytes was associated with upregulated NF-kappa B protein levels in a time-dependent fashion. Co-incubation of human chondrocytes with JNK and p38 inhibitors lead to abrogated levels of NF-kappa B, indicating that these MAPKs are important in the activation of chondrocytes after stimulation with resistin. Similarly, ADAMTS-5 expression levels were abrogated when co-incubated with p38, NF-kappa B, JNK, MEK and PI3K inhibitors. Our results demonstrate that resistin, released from adipose tissue, may be involved in the development of RA and OA in obese patients through degradation of joint cartilage via ADAMTS-5 released from activated chondrocytes.