Abstract
Aberrant angiogenesis plays a role in the pathogenesis of Sjögren's syndrome (SS). The aim of this study was to compare the levels of vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF) in stimulatory parotid saliva and in serum in healthy subjects (HS), patients with primary SS (pSS) and secondary SS (sSS) and to evaluate the expression of EGF, proangiogenic VEGF165 and antiangiogenic VEGF165 b mRNA isoforms. Additionally, we determined the salivary levels of serine/arginine splicing factor (SRSF1), which regulates VEGF165 and VEGF165 b expression. The study comprised 34 women (16 with pSS and 18 with sSS) and healthy subjects for blood and saliva sampling. EGF and VEGF levels in saliva and serum and salivary SRSF1 levels were determined by enzyme-linked immunosorbent assay (ELISA). The expression of VEGF165 , VEGF165 b and EGF in peripheral blood mononuclear cells (PBMC) was evaluated by quantitative polymerase chain reaction (qPCR). There were no differences in the levels of EGF, VEGF, SRSF1 and in the expression of the EGF, VEGF165 and VEGF165 b between HS and SS patients, or between pSS and sSS patients. The salivary levels of VEGF165 and EGF were significantly higher in pSS, sSS and HS than serum levels. Levels of SRSF1 correlated positively with VEGF and EGF levels. Levels of EGF, VEGF and SRSF1 correlated with each other. The balance of VEGF isoforms is not disturbed in SS. Saliva is more sensitive for the detection of EGF and VEGF than serum, but salivary levels of those proteins are not representative for SS.
Highlights
Sjögren’s syndrome (SS) is a systemic autoimmune disease characterized by periductal mononuclear cell infiltrate in the salivary and lachrymal glands, autoimmunization, injuries to endothelial cells and their subsequent apoptosis.[1,2] Inflammatory cells secrete growth factors, proteases and cytokines that induce extracellular matrix degradation, endothelial cell growth and migration promoting angiogenesis
There were no differences in the levels of epidermal growth factor (EGF), vascular endothelial growth factor (VEGF), serine-rich protein splicing factor 1 (SRSF1) and in the expression of the EGF, VEGF165 and VEGF165 b between healthy subjects (HS) and SS patients, or between primary SS (pSS) and secondary SS (sSS) patients
The salivary levels of VEGF165 and EGF were significantly higher in pSS, sSS and HS than serum levels
Summary
Sjögren’s syndrome (SS) is a systemic autoimmune disease characterized by periductal mononuclear cell infiltrate in the salivary and lachrymal glands, autoimmunization, injuries to endothelial cells and their subsequent apoptosis.[1,2] Inflammatory cells secrete growth factors, proteases and cytokines that induce extracellular matrix degradation, endothelial cell growth and migration promoting angiogenesis. Angiogenic factors induce endothelial cells to express adhesive molecules, cytokines and chemokines, which have additional stimulatory effects on chronic inflammation.[3]. One of the major proangiogenic regulators is vascular endothelial growth factor (VEGF) It promotes the migration of inflammatory cells into the extracellular matrix by inducing vascular permeability and endothelial cell expression of adhesion molecules, of which elevated levels are observed in SS.[3] VEGF exerts its biological function by binding to its receptors: VEGFR-1, VEGFR-2 and VEGFR-3.4,5 The main isoform VEGF165 has 165 amino acids in the mature structure. Aberrant angiogenesis plays a role in the pathogenesis of Sjögren’s syndrome (SS)
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