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2009-10-28 - Colloque/Présentation - poster - Anglais - 1 page(s)

Decleves Anne-Emilie , Seqqat R., Nonclerq Denis, Caron Nathalie, Flamion B, "Focal Increases in Hyaluronan and CD44 Correlate with High Proliferative Activity and Fibrosis in Nephrotoxic-Induced Chronic Renal Failure" in : Annual meeting of the American Society of Nephrology, San Diego, USA, 2009

  • Codes CREF : Histologie (DI3212), Sciences biomédicales (DI3200), Néphrologie - urologie (DI3325), Physiologie pathologique (DI3250)
  • Unités de recherche UMONS : Biologie moléculaire (M122)
  • Instituts UMONS : Institut des Sciences et Technologies de la Santé (Santé)
  • Centres UMONS : Centre de Recherche UMONS-Ambroise Paré (UMHAP)

Abstract(s) :

(Anglais) Chronic renal alterations induced experimentally by nephrotoxic agents are characterized by structural and functional changes in each nephron, leading to heterogeneous renal hypertrophy. These alterations may further lead to the development of chronic renal failure (CRF). Among the factors potentially involved in the processes of inflammation, regeneration and fibrosis occurring in this experimental model, Hyaluronan (HA) and its main receptor, CD44, could be considered as suitable candidates. In the present study, we administered nephrotoxic agents by subcutaneous injection to Wistar rats (K2Cr2O7 + HgCl2). Surviving animals developed CRF, demonstrating both atrophic and hypertrophic changes in different segments of the nephron. Histological sections taken between 1 wk and 6 months after nephrotoxics injection were examined to assess tissue injury, tubular and interstitial cell proliferation, immunostaining of hyaluronan (HA) and its main receptor CD44, and fibrosis. One week after injury, tubular damage and regeneration were associated with large deposits of HA and abundant inflammatory cells in the peritubular matrix. CD44 was expressed in both lymphocytes and macrophages, as well as in undifferentiated, regenerative epithelial cells. At longer term, some altered proximal tubules regained a differentiated phenotype while progressively losing CD44 expression. Peritubular HA declined in parallel to progression of tubular repair. Strikingly, however, strong HA immunostaining was retained in areas of chronic tubular alterations, together with CD44 expression in cystic and atrophic tubules, focal proliferation of interstitial cells, and patchy fibrosis. Our data obtained in a realistic model of CRF suggest that HA and CD44 are involved in the proliferation of both tubular regenerative cells and interstitial cells, the latter being associated with patches of progressive fibrosis.

(Anglais) Chronic renal alterations induced experimentally by nephrotoxic agents are characterized by structural and functional changes in each nephron, leading to heterogeneous renal hypertrophy. These alterations may further lead to the development of chronic renal failure (CRF). Among the factors potentially involved in the processes of inflammation, regeneration and fibrosis occurring in this experimental model, Hyaluronan (HA) and its main receptor, CD44, could be considered as suitable candidates. In the present study, we administered nephrotoxic agents by subcutaneous injection to Wistar rats (K2Cr2O7 + HgCl2). Surviving animals developed CRF, demonstrating both atrophic and hypertrophic changes in different segments of the nephron. Histological sections taken between 1 wk and 6 months after nephrotoxics injection were examined to assess tissue injury, tubular and interstitial cell proliferation, immunostaining of hyaluronan (HA) and its main receptor CD44, and fibrosis. One week after injury, tubular damage and regeneration were associated with large deposits of HA and abundant inflammatory cells in the peritubular matrix. CD44 was expressed in both lymphocytes and macrophages, as well as in undifferentiated, regenerative epithelial cells. At longer term, some altered proximal tubules regained a differentiated phenotype while progressively losing CD44 expression. Peritubular HA declined in parallel to progression of tubular repair. Strikingly, however, strong HA immunostaining was retained in areas of chronic tubular alterations, together with CD44 expression in cystic and atrophic tubules, focal proliferation of interstitial cells, and patchy fibrosis. Our data obtained in a realistic model of CRF suggest that HA and CD44 are involved in the proliferation of both tubular regenerative cells and interstitial cells, the latter being associated with patches of progressive fibrosis.