Browsing by Author "Rouhrazi, H"

Now showing 1 - 2 of 2
  • No Thumbnail Available
    Item
    Histological Investigation of Experimentally Induced Diabetes Effects on the Distribution of Transforming Growth Factor (TGFβ), Nuclear Factor Kappa B (Nf-κB), Heat Schock 90β (Hsp90β) and E-cadherin Proteins in Testicular Tissue
    Toros, P; Oltulu, F; Tuglu, I; Uysal, A; Özçinar, E; Turgan, N; Rouhrazi, H; Aktug, H
    Diabetes is a metabolic disorder characterized by high blood sugar levels and it causes complications in many systems, including the reproductive system. As a result of diabetic conditions, one of the mechanisms that can cause repression of reproductive activity is testicular oxidant stress. The identification of diabetes on the cell signaling molecules axis is still under discussion. The aim of this study was to detennine the effect of Transfonning Growth Factor (TGF beta), Nuclear Factor kappa B (NF-kappa B), Heat-schock 90 beta (HSP90 beta) signal pathways and E-cadherin cell adhesion molecule on infertility in diabetic rat testicular tissue. In our study, includes histological, molecular and biochemical analysis of testicular tissue removed at the end of the 2 weeks experiment period. A total of 14 adult male rats were divided as control and diabetes. No intervention was given to 7 male rats in the control group. For the diabetic group, 7 male rats were injected by intraperitoneal with a single dose of 55 mg/kg streptozotocin (STZ). TGF beta, NF-kappa B, HSP90 beta and E-cadherin proteins were immunohistochemically studied to investigate possible tissue damage, inflanunatoly process, cell stabilization and integrity due to diabetes. In order to determine oxidant stress, lipid peroxidation product malondialdehyde (MDA), glutathione (GSH) and glutathione peroxidase (GPx) analyzes were performed. Fibrosis, inflammatory changes and loss of spermatogenetic series are prominent findings in the diabetic group. On analysis of all the samples with immunostaining, in the diabetic group, TGF beta and NF-kappa B inununoexpression significantly increased, while Hsp90 beta and E-cadherin immunoexpression significantly decreased compared with control groups. Experimental diabetes was found to cause fibrosis, inflammation, disrupting cell adhesion and stabilization in testicular tissue. These results suggest that cellular therapy studies are needed for possible damage.
  • No Thumbnail Available
    Item
    JAK/STAT pathway interacts with intercellular cell adhesion molecule (ICAM) and vascular cell adhesion molecule (VCAM) while prostate cancer stem cells form tumor spheroids
    Duzagac, F; Inan, S; Simsek, FE; Acikgoz, E; Guven, U; Khan, SA; Rouhrazi, H; Oltulu, F; Aktug, H; Erol, A; Oktem, G
    Purpose: JAK/STAT is an evolutionarily conserved pathway and very important for second messenger system. This pathway is important in malignant transformation and accumulated evidence indicates that this pathway is involved in tumorigenesis and progression of several cancers. It was possible to assume that activation of JAK/STAT pathway is associated with increase in the expressions of ICAM-1 and VCAM-1. In this study we hypothesized that when cells were maintained as spheroids or monolayers, the structure of cancer stem cells (CSCs) could show differentiation when compared with non-CSCs. Methods: DU-145 human prostate cancer cells were cultured using the Ege University molecular embryology laboratory medium supplemented with 10% fetal bovine serum. Clusters of differentiation 133 (CD133)(+high)/ CD44(+high) prostate CSCs were isolated from the DU145 cell line by using BD FACSAria. CD133(+)/CD44(+) CSCs were cultured until confluent with 3% noble agar. The expression of these proteins in CSCs and non-CSCs was analyzed by immunohistochemistry. Results : Different expression profiles were observed in the conventional two-dimensional (2D) and three-dimensional (3D) experimental model system when CSCs and non-CSCs were compared. Human prostate CSCs exhibited intense ICAM-1 and VCAM-1 immunoreaction when compared with non-CSCs. These findings were supported by the fact that VCAM-1 on the surface of cancer cells binds to its counter-receptor, the a4 beta 1 integrin (also known as very-late antigen, VLA-4), on metastasis-associated macrophages, triggering VCAM-1-mediated activation of the phosphoinositide 3-kinase growth and survival pathway in cancer cells. Conclusions: The results of this study showed that changes in JAK/STAT pathway are related with adhesion molecules and could affect cancer progression.