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SAT0223 Soluble Semaphorin 3A and Neuropilin-1: New Markers for Dysregulation of Angiogenesis in Systemic Sclerosis?
  1. A. Olewicz-Gawlik1,
  2. D. Sikorska2,
  3. W. Samborski2
  1. 1Department of Rheumatology and Clinical Immunology
  2. 2Department of Rheumatology and Rehabilitation, Poznan University of Medical Sciences, Poznan, Poland


Background Semaphorins, through interactions with their receptors- neuropilins, play critical roles in many biological processes such as the regulation of immunity, apoptosis, cell migration and angiogenesis. Systemic sclerosis (SSc) is an autoimmune disease, characterised by dysregulation of angiogenesis, leading to severe ischemia and loss of capillaries.

Objectives The aim of the study was to investigate if soluble semaphorin 3A and neuropilin-1 could be involved in the dysregulation of angiogenesis in systemic sclerosis.

Methods This was an investigator-initiated cross-sectional study. Serum samples obtained from 37 patients with systemic sclerosis (age 53 ± 9 years) and control serum samples obtained from 24 healthy individuals (age 51 ± 15 years) and 20 patients with Sjögren's syndrome (age 46 ± 9 years). Samples were analyzed for the presence of soluble semaphorin 3A and neuropilin-1 using enzyme-linked immunosorbent assays. The results were expressed as median and range and compared by Mann-Whitney U test. P≤0.05 were considered statistically significant.

Results Serum semaphorin 3A levels were significantly higher in patients with systemic sclerosis (median 1.81 ng/mL; range 0.43–4.72 ng/mL) versus healthy controls (median 0.21 ng/mL; range 0.16–0.28 ng/mL) (p<0.001). Neuropilin-1 levels were significantly increased (median 844.26 pg/mL; range 556.80–1271.54 pg/mL) in comparison to those detected in healthy controls (median 58.60 pg/mL; range 33.75–80.00 pg/mL) (p<0.001) and patients with Sjögren's syndrome (median 278 pg/mL; range 137.50–443.70 pg/mL) (p<0.001). There was tendency to higher values of neuropilin-1 in patients with long lasting illness (Spearman's; r=0.29, p=0.075).

Conclusions Our data show that semaphorin 3A and neuropilin-1 levels are significantly increased in patients with systemic scleroderma. Semaphorin 3A and neuropilin-1 may be involved in the modifications of neuro-vascular mechanisms leading to dysregulation of angiogenesis in systemic scleroderma.

Disclosure of Interest None declared

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