PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection

Permanent URI for this collectionhttps://hdl.handle.net/11147/7645

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  • Review
    Citation - WoS: 13
    Citation - Scopus: 13
    Oxygen Delivery Biomaterials in Wound Healing Applications
    (WILEY-V C H VERLAG GMBH, 2023) Bayraktar, Sema; Üstün, Cansu; Kehr, Nermin Seda
    Oxygen (O2) delivery biomaterials have attracted great interest in the treatment of chronic wounds due to their potential applications in local and continuous O2 generation and delivery, improving cell viability until vascularization occurs, promoting structural growth of new blood vessels, simulating collagen synthesis, killing bacteria and reducing hypoxia-induced tissue damage. Therefore, different types of O2 delivery biomaterials including thin polymer films, fibers, hydrogels, or nanocomposite hydrogels have been developed to provide controlled, sufficient and long-lasting O2 to prevent hypoxia and maintain cell viability until the engineered tissue is vascularized by the host system. These biomaterials are made by various approaches, such as encapsulating O2 releasing molecules into hydrogels, polymer microspheres and 3D printed hydrogel scaffolds and adsorbing O2 carrying reagents into polymer films of fibers. In this article, different O2 generating sources such as solid inorganic peroxides, liquid peroxides, and photosynthetic microalgae, and O2 carrying perfluorocarbons and hemoglobin are presented and the applications of O2 delivery biomaterials in promoting wound healing are discussed. Furthermore, challenges encountered and future perspectives are highlighted. Oxygen delivery (O2) biomaterials have attracted great interest in the treatment of chronic wounds due to their ability to continuously deliver oxygen and support cell viability. Therefore, various O2 generating sources such as solid inorganic peroxides, liquid peroxides and photosynthetic microalgae, and O2-carrying perfluorocarbons and hemoglobin are incorporated into different biomaterial networks for wound healing applications.image
  • Article
    Citation - WoS: 2
    Citation - Scopus: 3
    Nkx3.1 Expression Contributes To Epithelial-Mesenchymal Transition of Prostate Cancer Cells
    (American Chemical Society, 2023) Saydullaeva, Iroda; Debeleç Bütüner, Bilge; Korkmaz, Kemal Sami
    Studies demonstrate that inflammation synergizes with highgrade aggressive prostate tumor development and ultimately metastatic spread, in which a lot of work has been done in recent years. However, the clear mechanism of inflammation inciting prostate cancer remains largely uncharacterized. Our previous study has shown that the conditioned media (CM)-mediated LNCaP cell migration is partially correlated with the loss of expression of the tumor suppressor NKX3.1. Here, we continue to investigate the inflammation-mediated migration of prostate cancer cells, and the role of NKX3.1 in this process to gain insights into cell migration-related changes comprehensively. Earlier, the model of inflammation in the tumor micro environment have been optimized by our research group; here, we continue to investigate the time-dependent effect of CM exposure together with NKX3.1 changes, in which we observed that these changes play important roles in gaining heterogeneous epithelial-to-mesenchymal transition (EMT) phenotype. Hence, this is an important parameter of tumor progression; we depleted NKX3.1 expression using the CRISPR/Cas9 system and examined the migrating cell clusters after exposure to inflammatory cytokines. We found that the migrated cells clearly demonstrate reversible loss of E-cadherin expression, which is consistent with subsequent vimentin expression alterations in comparison to control cells. Moreover, the data suggest that the AR mediated transcriptional program also contributes to mesenchymal-to-epithelial transition (MET) in prostate cancer progression. Furthermore, the quantitative proteomic analysis showed that migrated subpopulations from the same cell line presented different phenotypes in which the proteins overexpressed are involved in cell metabolism and RNA processing. According to KEGG pathway analysis, the ABC transporters were found to be the most significant. Thus, the dynamic process of cellular migration favors diverse genetic compositions under changing tumor microenvironments. The different levels of invasiveness are supported by shifting the cells in between these EMT and MET phenotypes.
  • Article
    Citation - WoS: 1
    Citation - Scopus: 1
    Exposure To Fumes of a Vegetable Margarine for Frying: Respiratory Effects in an Experimental Model
    (American Chemical Society, 2023) Cimrin, Arif H.; Alpaydin, Aylin Ozgen; Ozbal, Seda; Toprak, Melis; Yılmaz, Osman; Uluorman, Funda; Ergur, Bekir Uğur; Gürel, Duygu; Sofuoğlu, Sait Cemil
    Deep frying is one of the strongest emission sources into indoor air. A vegetable margarine has recently been used in commercial kitchens. This study investigated the respiratory effects of exposure to its fumes in an experimental model. A setup with glass chambers was constructed. A chamber housed a fryer. The fumes were transported to the other chamber where 24 Wistar albino rats were placed in four randomized groups: acute, subacute, chronic, and control for the exposure durations. PM10 concentration in the exposure chamber was monitored to ensure occupational levels were obtained. Sacrification was performed 24 h after exposure. Lung, trachea, and nasal concha specimens were evaluated by two blinded histologists under a light microscope with hematoxylin–eosin. Mild mononuclear cell infiltration, alveolar capillary membrane thickening, alveolar edema, and diffuse alveolar damage, along with diffuse hemorrhage, edema, and vascular congestion in the interstitium were observed in the acute and subacute groups, and were overexpressed in the chronic group, whereas normal lung histology was observed in the control group. The results indicate that exposure to fumes of vegetable margarine for frying in commercial kitchens may cause pulmonary inflammation that becomes severe as the duration of the exposure increases.
  • Article
    Citation - WoS: 44
    Citation - Scopus: 42
    Inflammation-Mediated Abrogation of Androgen Signaling: an in Vitro Model of Prostate Cell Inflammation
    (John Wiley and Sons Inc., 2014) Debeleç Bütüner, Bilge; Alapınar, Cansu; Varışlı, Lokman; Erbaykent Tepedelen, Burcu; Hamid, Syed Muhammad; Gönen Korkmaz, Ceren; Korkmaz, Kemal Sami
    As a link between inflammation and cancer has been reported in many studies, we established an in vitro model of prostatic inflammation to investigate the loss of androgen receptor (AR)-mediated signaling in androgen responsive prostate cell lines. First, the U937 monocyte cell line was differentiated into macrophages using phorbol acetate (PMA), and cells were induced with lipopolysaccharide (LPS) for cytokine secretion. Next, the cytokine levels (TNFα, IL-6, and IL1β) in conditioned media (CM) were analyzed. Prostate cells were then fed with CM containing varying concentrations of TNFα, and IkB degradation, nuclear factor kappa B (NFκB) translocation and transactivation, and the expression of matrix metalloproteinase-8 (MMP8) and matrix metalloproteinase-9 (MMP9) were then assessed. As a result of CM treatment, ubiquitin-mediated AR degradation, which was restored using anti-TNFα antibody neutralization, led to both a decrease in KLK4, PSA, and NKX3.1 expression levels and the upregulation of GPX2. In addition to the loss of AR, acute and chronic CM exposure resulted in p53 degradation and consequent p21 downregulation, which was also restored by either androgen administration or ectopic NKX3.1 expression via the stabilization of MDM2 levels in LNCaP cells. Additionally, CM treatment enhanced H2AX(S139) phosphorylation (a hallmark of DNA damage) and genetic heterogeneity in the absence of androgens in prostate cells without activating mitochondrial apoptosis. Thus, the data suggest that inflammatory cytokine exposure results in the loss of AR and p53 signaling in prostate cells and facilitates genetic heterogeneity via ROS accumulation to promote prostate carcinogenesis.