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Aetiopathogenesis

 

Different contributions of angiostatin and endostatin in angiogenesis impairment in systemic sclerosis: a cohort study

1, 2, 3, 4, 5

 

  1. Clinical Immunology Unit, Dept.
 of Medicine, Hosp. de Santo António (HSA), Centro Hospitalar do Porto (CHP); and Multidisciplinary Unit for Biomedical Investigation (UMIB), Instituto de Ciências Biomédicas Abel Salazar (ICBAS), Univ. do Porto, Portugal.
  2. Clinical Immunology Unit, Department of Medicine, Centro Hospitalar do Porto, Porto, Portugal.
  3. Laboratory of Cytometry, Dept. of Haematology, Hospital de Santo António (HSA), Centro Hospitalar do Porto (CHP); and Multidisciplinary Unit for Biomedical Investigation (UMIB), Inst. de Ciências Biomédicas Abel Salazar (ICBAS), Univ. do Porto, Portugal.
  4. Department of Vascular Surgery, Centro Hospitalar do Porto, Porto, Portugal.
  5. Clinical Immunology Unit, Dept.
 of Medicine, Hosp. de Santo António (HSA), Centro Hospitalar do Porto (CHP); and Multidisciplinary Unit for Biomedical Investigation (UMIB), Instituto de Ciências Biomédicas Abel Salazar (ICBAS), Univ. do Porto, Portugal.

CER8981
2016 Vol.34, N°5 ,Suppl.100
PI 0037, PF 0042
Aetiopathogenesis

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PMID: 26885625 [PubMed]

Received: 16/09/2015
Accepted : 14/12/2015
In Press: 16/02/2016
Published: 13/10/2016

Abstract

OBJECTIVES:
To determine the concentrations of circulating endostatin and angiostatin in patients with systemic sclerosis (SSc) and to assess its relationship to disease subsets, evolution phase, organ involvement and nailfold capillaroscopic changes.
METHODS:
Endostatin and angiostatin serum levels were measured by ELISA in a cohort of 57 patients with SSc, and correlated with disease subsets, evolution phase, organ involvement and nailfold capillaroscopic changes.
RESULTS:
Endostatin and angiostatin serum levels were significantly higher in patients with SSc than in healthy controls. Also, angiostatin was elevated in diffuse cutaneous SSc (dcSSc) and limited cutaneous SSc (lcSSc), but not in pre-SSc, while endostatin was increased in all SSc subsets. Moreover, endostatin was augmented in lcSSc, with or without CREST syndrome, whereas angiostatin was increased exclusively in patients with CREST. Analysis according to disease evolution phase found that endostatin was elevated in all phases while angiostatin was only significantly higher in intermediate and late phases of disease. Analysis regarding organ involvement revealed that angiostatin was significantly higher in patients with osteoarticular involvement and with more serious lung affection; no significant differences were found for endostatin. Finally, endostatin was significantly increased in all nailfold capillaroscopy stages, while angiostatin was only elevated in active and late phases.
CONCLUSIONS:
In accordance with previous studies, we found that endostatin and angiostatin concentrations are elevated in SSc patients. Additionally, we recognised the important role that endostatin might play as an early disease marker and realized that angiostatin is a marker of late disease and relates to lung disease severity.

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