Serotoninin Renal Hasardaki Rolü
Özet
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.
