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Increased sensitivity to extracellular ATP of fibroblasts from patients affected by systemic sclerosis
  1. Andrea Lo Monaco1,
  2. Sara Gulinelli2,
  3. Gabriella Castellino1,
  4. Anna Solini3,
  5. Davide Ferrari2,
  6. Renato La Corte1,
  7. Francesco Trotta1,
  8. Francesco Di Virgilio2
  1. 1Department of Clinical and Experimental Medicine, Section of Rheumatology, University of Ferrara, Ferrara, Italy
  2. 2Department of Experimental and Diagnostic Medicine, Section of General Pathology, University of Ferrara, Ferrara, Italy
  3. 3Department of Internal Medicine, University of Pisa, Pisa, Italy
  1. Correspondence to:
    Andrea Lo Monaco
    MD, PhD, Azienda Universitaria-Ospedaliera S. Anna, C.so della Giovecca n. 203, Ferrara 44100; lmnndr{at}unife.it

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Systemic sclerosis (SSc) is an autoimmune disease characterised by an excessive production of collagen and other constituents of the extracellular matrix in the skin, lung and other internal organs, by damage of the microvascular endothelium, and dysregulation of cytokine secretion.1–3 Recent studies show that extracellular nucleotides trigger cytoplasmic Ca2+ increases ([Ca2+]i), morphological changes and cytokine secretion in human fibroblasts.4 Nucleotides are released in response to traumas or inflammation, thus they may also affect fibroblast responses in scleroderma.5

We investigated intracellular second-messenger generation, cytokine secretion and morphological changes in involved, non-atrophic skin biopsies from five patients with the diffuse form of SSc.6 Fibroblasts from patients with SSc had a high rate of spontaneous interleukin (IL)-6 release, which was further enhanced by stimulation …

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