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Endothelin and sex hormones modulate the fibronectin synthesis by cultured human skin scleroderma fibroblasts
  1. S Soldano (stesoldo{at}yahoo.it)
  1. Research Laboratories and Clinical Academic Unit of Rheumatology, University of Genova, Italy
    1. P Montagna
    1. Research Laboratories and Clinical Academic Unit of Rheumatology, University of Genova, Italy
      1. B Villaggio
      1. Research Laboratories and Clinical Academic Unit of Nefrology, University of Genova, Italy
        1. A Parodi
        1. Department of Endocrinological and Medical Science, Unit of Dermatology, University of Genova, Italy
          1. G Gianotti
          1. Department of Endocrinological and Medical Science, Unit of Dermatology, University of Genova, Italy
            1. A Sulli (albertosulli{at}unige.it)
            1. Research Laboratories and Clinical Academic Unit of Rheumatology, University of Genova, Italy
              1. B Seriolo
              1. Research Laboratories and Clinical Academic Unit of Rheumatology, University of Genova, Italy
                1. ME Secchi
                1. Research Laboratories and Clinical Academic Unit of Rheumatology, University of Genova, Italy
                  1. M Cutolo (mcutolo{at}unige.it)
                  1. Research Laboratories and Clinical Academic Unit of Rheumatology, University of Genova, Italy

                    Abstract

                    Objective: To evaluate the influence of endothelin-1 (ET-1) and sex hormones on cell proliferation and extracellular matrix (ECM) synthesis (i.e. fibronectin, laminin) by cultured normal and scleroderma (SSc) human skin fibroblasts (FB).

                    Methods: Primary cultures of FB were treated with ET-1 and sex hormones (17 beta-estradiol or testosterone) for 24 hours. Cell growth was analysed by methiltetrazolium salt test, ECM synthesis was evaluated by immunocytochemistry and Western blot, both at 24 hours.

                    Results: In normal FB, ET-1 and 17beta-estradiol, as well as their combination, increased cell growth (p<0.001, p<0.001, p<0.01 vs untreated cells (cnt), respectively) and fibronectin synthesis (p<0.05, p<0.05, p<0.01 vs cnt, respectively). On the contrary, testosterone either alone or in combination with ET-1 did not influence cell proliferation, but decreased fibronectin synthesis (p<0.05, testosterone vs cnt). In SSc FB, ET-1 and 17beta-estradiol alone or their combination induced an increased fibronectin synthesis (p<0.05, p<0.05, p<0.01 vs cnt, respectively). Unexpectedly, testosterone induced an increase of fibronectin synthesis (p<0.05 vs cnt).

                    Conclusions: In conclusion, both ET-1 and 17beta-estradiol seem to exert a profibrotic effect in both normal and SSc cultured FB and might suggest their synergistic effect in the pathogenesis of the fibrotic process in SSc.

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