Journal Article

Polycystin‐2 expression is increased following experimental ischaemic renal injury

Yan Zhao, John L. Haylor and Albert C. M. Ong

in Nephrology Dialysis Transplantation

Published on behalf of European Renal Association - European Dialysis and Transplant Assoc

Volume 17, issue 12, pages 2138-2144
Published in print December 2002 | ISSN: 0931-0509
Published online December 2002 | e-ISSN: 1460-2385 | DOI: http://dx.doi.org/10.1093/ndt/17.12.2138
Polycystin‐2 expression is increased following experimental ischaemic renal injury

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Background. Mutations in PKD2 account for 15% of patients with autosomal dominant polycystic kidney disease. Expression of the PKD2 protein, polycystin‐2, is developmentally regulated, suggesting a major role for this protein during nephrogenesis. However, the regulation of polycystin‐2 expression in the adult kidney has not been previously explored.

Methods. We have utilized an established model of renal ischaemic injury to study polycystin‐2 expression in adult rat kidney for up to 120 h following ischaemia.

Results. Our results indicate that polycystin‐2 expression is increased in the post‐ischaemic kidney by up to 5‐fold, with a peak in expression at 48 h reperfusion. This time course mirrored the increase in cell proliferation observed. In the non‐ischaemic kidney, polycystin‐2 expression was highest in distal nephron segments but faint proximal tubular staining was also observed. No expression was seen in glomeruli. In the ischaemic kidney, polycystin‐2 expression was greatly increased but the increase in expression was not restricted to segments with the highest number of proliferating cells. Moreover, polycystin‐2 was detectable mainly intracellularly following ischaemia. Consistent with this, polycystin‐2 was completely sensitive to endoglycosidase H during renal recovery, suggesting that it remains largely retained within the endoplasmic reticulum under these conditions.

Conclusions. Our results provide the first evidence that polycystin‐2 is increased following renal ischaemia, but show that this increase is not restricted to actively proliferating cells. The increase in polycystin‐2 may relate instead to the process of cellular repair or differentiation following injury.

Keywords: ADPKD; PKD2; polycystic kidney disease; polycystin‐2; renal ischaemia

Journal Article.  3567 words.  Illustrated.

Subjects: Nephrology

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