Yazar "Pektanc, Gulsum" seçeneğine göre listele

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    Altered Expression of ADAMTSs and HAPLNs in Preeclamptic Placenta
    (Aves, 2018) Kandemir, Sevgi Irtegun; Taskin, Irmak Icen; Pektanc, Gulsum; Tekin, Mehmet Ali; Demircan, Kadir
    Objective: Preeclampsia (PE) is a pregnancy-specific complication defined by the new onset of hypertension and proteinuria during the second trimester of pregnancy. The pathogenesis of PE remains poorly understood. Revealing the key factors involved in placental dysfunction is critical for the understanding the pathogenesis of PE. The aim of this study was to determine the expression levels of ADAMTSs and their molecular partners, TIMP-3 and HAPLNs in the placental tissues of women with PE. Materials and Methods: Experimental research was conducted on control and preeclamptic placentas. A total of 10 control and 10 preeclamptic placentas were included in the present study. The expression levels of ADAMTSs, HAPLNs, and TIMP-3 were analyzed in two groups by Western blot. Results: The expression levels of ADAMTS-4, -8, -10, -12, -13, -14, -16, and -19 were considerably lower, whereas the expression levels of HAPLN-1, -2, and -4; ADAMTS-18; and TIMP-3 were significantly higher in preeclamptic placentas than in controls. Conclusion: Altered expression levels of ADAMTSs and their molecular partners, TIMP-3 and HAPLNs, may contribute to the pathogenesis of PE.
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    Deregulation of c-Src tyrosine kinase and its downstream targets in pre-eclamptic placenta
    (Wiley, 2017) Irtegun, Sevgi; Akcora-Yildiz, Dilara; Pektanc, Gulsum; Karabulut, Cagla
    AimPre-eclampsia is a serious pregnancy disorder characterized by the new onset of hypertension and proteinuria in the second trimester of pregnancy. The determination of a key signaling regulatory mechanism involved in placental functions is critical to understanding the pathogenesis of pre-eclampsia. The aim of this study was to examine the activity of c-Src and its downstream targets, extracellular signal-regulated kinase 1/2, p38 and Jun N-terminal kinase, as well as nuclear factor (NF)-?B in placental tissues collected from women with pre-eclampsia. MethodsTen pre-eclamptic (PE) placentas and 10 control placentas were used in this study. The Western blot method was performed to evaluate the c-Src/ mitogen activated protein kinase/NF-?B signaling pathway in each group. Resultsc-Src phosphorylation at Tyr-416, used as a measure of c-Src activity, was significantly decreased in PE placentas relative to the control. Reduced c-Src activity resulted in the suppression of extracellular signal-regulated kinase 1/2 phosphorylation and a significant reduction in the phosphorylation of p38 and Jun N-terminal kinase in PE placentas. Moreover, I?B phosphorylation was significantly elevated, while NF-?B phosphorylation was suppressed in PE placentas. ConclusionsThe c-Src/MAPK/NF-?B signaling pathway may contribute to the pathogenesis of pre-eclampsia.
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    Pharmacological Inactivation of Src Family Kinases Inhibits LPS-Induced TNF-? Production in PBMC of Patients with Behcet's Disease
    (Hindawi Ltd, 2016) Irtegun, Sevgi; Pektanc, Gulsum; Akkurt, Zeynep M.; Bozkurt, Mehtap; Turkcu, Fatih M.; Kalkanli-Tas, Sevgi
    Behcet's disease (BD) is a multisystemic chronic inflammatory disease characterized by relapsing oral and genital ulcers, uveitis, and skin lesions. The pathogenesis of BD is still unknown. Aberrant production of some cytokines/chemokines plays an important role in the pathogenesis of various inflammatory diseases. Revealing a key signaling regulatory mechanism involved in proinflammatory cytokines/chemokines production is critical for understanding of the pathogenesis of BD. The aim of this study was to determine the role of Src family kinases (SFKs) in production of some LPS-induced proinflammatory cytokines/chemokines in peripheral blood mononuclear cells (PBMC) of active BD patients. Chemical inhibition of SFKs activity impaired LPS-induced TNF-alpha production in PBMC of active BD patients, suggesting that modulating SFKs activity may be a potential target for BD treatment.
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    Polymorphism in the second intron of the FGFR2 gene rs1219648 associated with the early-onset breast cancer in Turkish population
    (E-Century Publishing Corp, 2017) Taskin, Irmak Icen; Tekin, Mehmet A.; Pektanc, Gulsum; Munzuroglu, Omer; Kandemir, Sevgi Irtegun
    The incidence of early-onset breast cancer has been increased up to 25% in the developing countries. Several studies reported that breast cancer cases in younger women have different biological characteristics than others. These patients should be studied separately. Lack of the necessary information about the younger patients prevents significant improvements about diagnosis and treatment strategies targeting these patients. Polymor-phisms within intron 2 of the FGFR2 gene have been associated with postmenopausal breast cancer patients in many populations. However, there exists no research on the impact of rs1219648 on early-onset breast cancer in Turkish population. In this study, the association of rs1219648 with early-onset breast cancer in Turkish women has been investigated. A total of 171 subjects, including 75 female breast cancer patients who were less than or equal to 40 years of age and 96 age-matched healthy controls were recruited. Our results indicate that G allele of the rs1219648 is statistically correlated with early-onset breast cancer (OR 2.0098, 95% CI 1.3016-3.1032, P=0.002). When rs1219648 was examined as a categorical variable where the reference category related to the wild-type genotype (AA), the calculated OR was [2.112 (95% CI 0.9904-4.5058), P= 0.053], and [5.2308 (95% CI 1.939114.1102), P=0.001], for genotypes AG and GG, respectively. We present the first report on FGFR2 rs1219648 polymorphism in early-onset breast cancer in Turkish women. Our results propose that rs1219648 polymorphism individually confers susceptibility for development of early-onset breast cancer in the Turkish populations.