NDT Advance Access published online on June 4, 2006
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfl179
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1 Instituto ‘Reina Sofía’ de Investigación Nefrológica and Departamento de Fisiología & Farmacología, Universidad de Salamanca, Salamanca, Spain
* To whom correspondence should be addressed. Background. Renal ischaemia-reperfusion (I-R) can cause acute tubular necrosis and chronic renal deterioration. Endoglin, an accessory receptor for Transforming Growth Factor- Methods. Endoglin expression was monitored over 14 days after renal I-R in rats. As endoglin-null mice are not viable, the role of endoglin in I-R was studied by comparing renal I-R injury in haploinsufficient mice (Eng+/-) and their wild-type littermates (Eng+/+). Renal function, morphology and molecular markers of acute renal injury and inflammation were compared. Results. Endoglin mRNA up-regulation in the post-ischaemic kidneys of rats occurred at 12 h after I-R; endoglin protein levels were elevated throughout the study period. Expression was initially localized to the vascular endothelium, then extended to fibrotic and inflamed areas of the interstitium. Two days after I-R, plasma creatinine elevation and acute tubular necrosis were less marked in Eng+/- than in Eng+/+ mice. Significant up-regulation of endoglin protein was found only in the post-ischaemic kidneys of Eng+/+ mice and coincided with an increased mRNA expression of the TGF- Conclusions. Endoglin is up-regulated in the post-ischaemic kidney and endoglin-haploinsufficient mice are protected from renal I-R injury. Endoglin may play a primary role in promoting inflammatory responses following renal I-R.
Received June 9, 2005
Accepted March 20, 2006
Original Article
Endoglin regulates renal ischaemia-reperfusion injury
Neil G. Docherty 1,
José M. López-Novoa 1 *,
Miguel Arevalo 2,
Annette Düwel 1,
Ana Rodriguez-Peña 1,
Fernando Pérez-Barriocanal 1,
Carmelo Bernabeu 3,
and
Nélida Eleno 1
2 Departamento de Anatomía e Histología Humanas, Universidad de Salamanca, Salamanca, Spain
3 Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas, Madrid, Spain
José M. López-Novoa, E-mail: jmlnovoa{at}usal.es
Abstract 
1 (TGF-1), is expressed on activated endothelium during macrophage maturation and implicated in the control of fibrosis, angiogenesis and inflammation.1 and collagen IV (
1) chain genes. Significant increases in vascular cell adhesion molecule-1 (VCAM-1) and inducible nitric oxide synthase (iNOS) expression, nitrosative stress, myeloperoxidase activity and CD68 staining for macrophages were evident in post-ischaemic kidneys of Eng+/+, but not Eng+/- mice, suggesting that impaired endothelial activation and macrophage maturation may account for the reduced injury in post-ischaemic kidneys of Eng+/- mice.1.
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