Serotoninin Renal Hasardaki Rolü
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In various acute and chronic renal diseases, tissue damage occurs and platelet activation is observed. Recent studies suggest that some factors released from activated platelets may participate in inflammation and fibrosis observed after renal injury. Serotonin is stored in platelets and is released upon platelet activation into the local microenvironment. Serotonin is released upon platelet activation and its effect on proximal tubular epithelial cells has not been determined yet. In this thesis, it was investigated whether platelets and platelet-released serotonin are involved in the function of renal proximal tubular epithelial cells. For this purpose, renal proximal tubular epithelial epithelial cells were stimulated with various concenrations of platelet lysate (PL) or serotonin for different periods and the phenotypic transition of these cells into myofibroblasts were demonstrated under light microscobe. This transition is confirmed by the determination of upregulation in α-SMA gene expression, which is known as fibroblast-myofibroblast transdifferantiation marker. Martix metalloproteinase-2 (MMP-2), tissue inhibitors of metalloproteinase-1 (TIMP-1) and collagen-α1 (COL-α1) upregulations in gene and protein levels, which are reported to be changed in renal inury, were also demonstrated. After stimulation with serotonin and PL, expressions of some inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and transforming growth factor-β1 (TGF-β1) were increased in both protein and gene levels. Recently, there isn’t any published report on the effect of serotonin on renal injury. Platelets are known as the cells that aggregate in the injury site in the early stage and serotonin is released in excess amounts into the local microenvironment following the activation. Therefore it is important to define the role of serotonin both in damage and in healing process.