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2005-11-08 - Colloque/Présentation - poster - Anglais - 1 page(s)

Decleves Anne-Emilie , Caron Nathalie, Nonclerq Denis, Toubeau Gerard, Legrand Alexandre , Flamion B, "Association of CD44 and hyaluronan with inflammatory and tubular cells in the postischemic kidney." in Annual meeting of the American Society of Nephrology, , 16, 431A, Philadelphia, USA, 2005

  • Codes CREF : Biochimie (DI3112), Histologie (DI3212), 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) Urotensin II (UII) was recently identifi ed in mammals as a potential modulator of vascular tone by activating a specifi c receptor UT-R. However, little is known about the functional relevance of this peptide. Since it was reported that plasma UII increased in patients with chronic renal failure (CRF), our aim was to characterize the intrarenal distribution and regulation of UII and UT-R in rats with normal renal function (Sham) or CRF, achieved by 5/6 nephrectomy (5/6Nx). In vivo experiments were also undertaken in anesthetized rats to evaluate the hemodynamic and renal effects of an intrarenal infusion of UII (20 ng/kg/min). Immunohistochemistry and analysis of mRNA expression for UII and UT-R using quantitative RT-PCR (Taqman) were performed on kidneys from Sham and 5/6Nx rats. Intrarenal distribution of UII and UT-R in normal tissue is summarized in the following table.In 5/6Nx rats, UII-like immunoreactivity remained almost unaffected. A signifi cant reduction of UT-R immunostaining in the inner stripe of outer medulla was confi rmed by a four-fold decrease in UT-R mRNA in this area (P<0.05). In Sham rats (n=6), infusion of UII decreased mean arterial pressure, renal blood fl ow and glomerular fi ltration rate by 10, 17 and 11% (P<0.05), as well as diuresis and natriuresis by 30 and 40% (P<0.05). Interestingly, these variables were not modifi ed by UII in 5/6Nx rats (n=6). In summary, UT-R and UII-like immunoreactivity was present in normal and 5/6Nx rat kidneys, their mutually exclusive localization further suggesting a paracrine way of action for UII. Moreover, UII was shown to modulate in vivo hemodynamic and excretory functions of the normal kidney. Interestingly, the blunted effects of UII in 5/6Nx rats, that could be linked to a down-regulation of UT receptors, indicate that the functionality of this system could be altered in rats with CRF.

(Anglais) Hyaluronan (HA) and its receptor CD44 accumulate in the kidney after acute ischemiareperfusion injury (I/R), with different time-courses and localizations. Recently, CD44 deficiency was shown to decrease neutrophil influx into the postischemic kidney (JASN 2005). On the other hand, resolution of inflammation and HA clearance are delayed in CD44-/- mice suffering renal or lung injury. Using immunohistochemistry, we examined the association of CD44 and HA with inflammatory and tubular cells during a 30 days (d) period in uninephrectomized rats submitted to a 60 min renal ischemia. Inflammatory cells. After I/R, all infiltrating neutrophils expressed CD44 with a peak in outer stripe of outer medulla (OS) at 48h. Besides, monocytes-macrophages were detected in isolation or in granulomas from 48h to 7d, but only some expressed CD44. Some non-leucocytic interstitial cells also expressed CD44. Tubular cells. CD44 stained mainly the basal membrane of collecting ducts in the inner stripe of control rats. After I/R, CD44 extended to the apical pole while AQP3 was downregulated and remained basolateral. Proximal tubules also acquired CD44 during regenerative processes, with a delay (peak at 7d) compared to PCNA staining (mostly + at 48h). Later, remodeling areas were strongly + for CD44, which by 30d had vanished from regenerated tubules. Hyaluronan. HA appeared in the extracellular matrix of cortex and OS at 12h after I/R, progressively filled and distorted the interstitium, and persisted for ≥30d in remodeling zones. Moreover, the HA glue seemingly filled with interstitial, possibly moving cells. Conclusion. Our detailed observations reveal that de novo or modified CD44 expression is a feature of several cell types after I/R. In tubular cells and infiltrated neutrophils, CD44 may be associated with apoptosis rather than with proliferation, and it may help clear neutrophils and HA. The reason for maintenance of abundant interstitial HA in remodeling areas is unclear but it may play a role in subsequent development of fibrosis.

(Anglais) Urotensin II (UII) was recently identifi ed in mammals as a potential modulator of vascular tone by activating a specifi c receptor UT-R. However, little is known about the functional relevance of this peptide. Since it was reported that plasma UII increased in patients with chronic renal failure (CRF), our aim was to characterize the intrarenal distribution and regulation of UII and UT-R in rats with normal renal function (Sham) or CRF, achieved by 5/6 nephrectomy (5/6Nx). In vivo experiments were also undertaken in anesthetized rats to evaluate the hemodynamic and renal effects of an intrarenal infusion of UII (20 ng/kg/min). Immunohistochemistry and analysis of mRNA expression for UII and UT-R using quantitative RT-PCR (Taqman) were performed on kidneys from Sham and 5/6Nx rats. Intrarenal distribution of UII and UT-R in normal tissue is summarized in the following table.In 5/6Nx rats, UII-like immunoreactivity remained almost unaffected. A signifi cant reduction of UT-R immunostaining in the inner stripe of outer medulla was confi rmed by a four-fold decrease in UT-R mRNA in this area (P<0.05). In Sham rats (n=6), infusion of UII decreased mean arterial pressure, renal blood fl ow and glomerular fi ltration rate by 10, 17 and 11% (P<0.05), as well as diuresis and natriuresis by 30 and 40% (P<0.05). Interestingly, these variables were not modifi ed by UII in 5/6Nx rats (n=6). In summary, UT-R and UII-like immunoreactivity was present in normal and 5/6Nx rat kidneys, their mutually exclusive localization further suggesting a paracrine way of action for UII. Moreover, UII was shown to modulate in vivo hemodynamic and excretory functions of the normal kidney. Interestingly, the blunted effects of UII in 5/6Nx rats, that could be linked to a down-regulation of UT receptors, indicate that the functionality of this system could be altered in rats with CRF.