DI-UMONS : Dépôt institutionnel de l’université de Mons

Recherche transversale
Rechercher
(titres de publication, de périodique et noms de colloque inclus)
2009-11-02 - Colloque/Présentation - poster - Anglais - 1 page(s)

Decleves Anne-Emilie , Voisin V, Bouby N, Kultti Anne, Tammi Markku, Flamion B, Caron Nathalie, "Sequential Hyaluronan Accumulation and Fragmentation in Rat Kidney Ischemia-Reperfusion Injury." in Annual meeting of the American Society of Nephrology, San Diego, USA, 2009

  • Codes CREF : Biochimie (DI3112), Histologie (DI3212), Sciences biomédicales (DI3200), Néphrologie - urologie (DI3325), Physiologie pathologique (DI3250), Métabolisme (DI3223)
  • 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) Hyaluronan (HA) accumulation and small-size HA fragments have been linked to key inflammatory processes including in vitro toll-like receptor activation. However, the precise time-course and determinants of HA fragmentation in vivo remain unknown. Therefore, the expression and activity of the main HA synthases (HAS1, HAS2, HAS3) and hyaluronidases (HYAL1, HYAL2) were assessed by real-time PCR, immunohistochemistry and zymography in the outer [OSOM] and inner stripe [ISOM] of the outer medulla for two weeks after severe ischemia and reperfusion in rats. HA was extracted and its fragmentation was evaluated by membrane filtration and size-exclusion chromatography. Within one day, HAS1 mRNA was up-regulated more than 50- and 35-fold in OSOM and ISOM, respectively. Thereafter it tended to normalize while HAS2 increased steadily. Both enzymes were localized around tubules and in the interstitium. HYAL1 and HYAL2 were strongly but transiently repressed. In line with these changes, HA accumulated at Day 1 mostly as high molecular weight (MW) species with an elution profile similar to a reference 2,500-kDa HA, and at Day 14 mostly as medium- to low-size fragments: their increase vs baseline averaged ×80 in OSOM and ×6 in ISOM. We have thus shown that HA accumulation in renal ischemia-reperfusion involves two steps. Within 24 h, massive activation of HAS1 combined with repression of HYAL1 and HYAL2 leads to a pool of high-MW HA. Later, smaller-size HA predominates following HAS2 induction and hyaluronidase reactivation. These events condition the inflammatory environment and are amenable to pharmacological manipulations.