Browsing by Author "Candar, Tuba"

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    Behcet's: A Disease or a Syndrome? Answer from an Expression Profiling Study
    (2016) Oguz, Ali Kemal; Yilmaz, Seda Tasir; Oygur, Cagdas Sahap; Candar, Tuba; Sayin, Irmak; Kilicoglu, Sibel Serin; Ergun, Ihsan; Ates, Askin; Ozdag, Hilal; Akar, Nejat; 26890122
    Behcet's disease (BD) is a chronic, relapsing, multisystemic inflammatory disorder with unanswered questions regarding its etiology/pathogenesis and classification. Distinct manifestation based subsets, pronounced geographical variations in expression, and discrepant immunological abnormalities raised the question whether Behcet's is "a disease or a syndrome". To answer the preceding question we aimed to display and compare the molecular mechanisms underlying distinct subsets of BD. For this purpose, the expression data of the gene expression profiling and association study on BD by Xavier et al (2013) was retrieved from GEO database and reanalysed by gene expression data analysis/visualization and bioinformatics enrichment tools. There were 15 BD patients (B) and 14 controls (C). Three subsets of BD patients were generated: MB (isolated mucocutaneous manifestations, n = 7), OB (ocular involvement, n = 4), and VB (large vein thrombosis, n = 4). Class comparison analyses yielded the following numbers of differentially expressed genes (DEGs); B vs C: 4, MB vs C: 5, OB vs C: 151, VB vs C: 274, MB vs OB: 215, MB vs VB: 760, OB vs VB: 984. Venn diagram analysis showed that there were no common DEGs in the intersection "MB vs C" boolean AND "OB vs C" boolean AND "VB vs C". Cluster analyses successfully clustered distinct expressions of BD. During gene ontology term enrichment analyses, categories with relevance to IL-8 production (MB vs C) and immune response to microorganisms (OB vs C) were differentially enriched. Distinct subsets of BD display distinct expression profiles and different disease associated pathways. Based on these clear discrepancies, the designation as "Behcet's syndrome" (BS) should be encouraged and future research should take into consideration the immunogenetic heterogeneity of BS subsets. Four gene groups, namely, negative regulators of inflammation (CD69, CLEC12A, CLEC12B, TNFAIP3), neutrophil granule proteins (LTF, OLFM4, AZU1, MMP8, DEFA4, CAMP), antigen processing and presentation proteins (CTSS, ERAP1), and regulators of immune response (LGALS2, BCL10, ITCH, CEACAM8, CD36, IL8, CCL4, EREG, NFKBIZ, CCR2, CD180, KLRC4, NFAT5) appear to be instrumental in BS immunopathogenesis.
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    Galectin-3, IL-1A, IL-6, and EGF Levels in Corneal Epithelium of Patients With Recurrent Corneal Erosion Syndrome
    (2020) Candar, Tuba; Asena, Leyla; Alkayid, Husamadden; Altinors, Dilek D.; 0000-0001-5223-0279; 0000-0002-6848-203X; 32732704; E-5914-2016; AAK-8077-2021
    Purpose: To determine the galectin-3 (Gal3), interleukin-1 (IL-1), interleukin-6 (IL-6), and epidermal growth factor (EGF) levels in corneal epithelium of patients with recurrent corneal erosion (RCE) syndrome and compare them with healthy controls. Methods: In this prospective interventional case control study, 32 eyes of 32 patients with RCE syndrome who had corneal epithelial erosions and 28 eyes of 28 healthy participants scheduled for photorefractive keratectomy (control group) were included. Exclusion criteria included corneal dystrophies, ectasia, dry eye, previous ocular surgery or topical medications, and systemic diseases. Epithelial samples were obtained during epithelial debridement in the study group and mechanical epithelial keratectomy in the control group. Galectin-3 levels were studied by the chemiluminescent microparticle immunoassay method. IL-1, IL-6, and EGF levels were determined using corresponding ELISA kits. Results: The median Gal3 levels were 132.25 ng/mL in the study group and 106.50 ng/mL in the control group. The median IL-1 and IL-6 levels were 6.24 pg/mL and 10.16 pg/mL, respectively, in the study group which were higher than that in the control group. The median EGF level in the study group was lower than that the control group with 1.30 pg/mL versus 2.67 pg/mL. In the control group, there was a significant positive correlation between EGF and IL-6 (r = 0.554;P= 0.040). A similar correlation was not observed in patients with RCE (r = -0.071;P= 0.794). Conclusions: The lack of increased EGF expression and the imbalance between growth factors, adhesion molecules, and interleukins may be the reason for the impaired wound healing response in RCE syndrome.