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Int. J. Mol. Sci. 2016, 17(6), 802; doi:10.3390/ijms17060802

Kidney Injury Molecule-1 Is Specifically Expressed in Cystically-Transformed Proximal Tubules of the PKD/Mhm (cy/+) Rat Model of Polycystic Kidney Disease

1
Division of Nephrology, III. Medical Clinic, University Hospital Frankfurt, Goethe-University, 60590 Frankfurt, Germany
2
Department of Urology and Paediatric Urology, Philipps-University Marburg, 35043 Marburg, Germany
3
Medical Research Center, University of Heidelberg, 68167 Mannheim, Germany
*
Author to whom correspondence should be addressed.
Academic Editor: Alan Parrish
Received: 6 April 2016 / Revised: 15 May 2016 / Accepted: 18 May 2016 / Published: 24 May 2016
(This article belongs to the Special Issue Advances in Chronic Kidney Disease)
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Abstract

Expression of kidney injury molecule-1 (Kim-1) is rapidly upregulated following tubular injury, constituting a biomarker for acute kidney damage. We examined the renal localization of Kim-1 expression in PKD/Mhm (polycystic kidney disease, Mannheim) (cy/+) rats (cy: mutated allel, +: wild type allel), an established model for autosomal dominant polycystic kidney disease, with chronic, mainly proximal tubulointerstitial alterations. For immunohistochemistry or Western blot analysis, kidneys of male adult heterozygously-affected (cy/+) and unaffected (+/+) littermates were perfusion-fixed or directly removed. Kim-1 expression was determined using peroxidase- or fluorescence-linked immunohistochemistry (alone or in combination with markers for tubule segments or differentiation). Compared to (+/+), only in (cy/+) kidneys, a chronic expression of Kim-1 could be detected by Western blot analysis, which was histologically confined to an apical cellular localization in areas of cystically-transformed proximal tubules with varying size and morphology, but not in distal tubular segments. Kim-1 was expressed by cystic epithelia exhibiting varying extents of dedifferentiation, as shown by double labeling with aquaporin-1, vimentin or osteopontin, yielding partial cellular coexpression. In this model, in contrast to other known molecules indicating renal injury and/or repair mechanisms, the chronic renal expression of Kim-1 is strictly confined to proximal cysts. Its exact role in interfering with tubulo-interstitial alterations in polycystic kidney disease warrants future investigations. View Full-Text
Keywords: Kim-1; polycystic kidney; rat model; proximal tubule; dedifferentiation Kim-1; polycystic kidney; rat model; proximal tubule; dedifferentiation
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Gauer, S.; Urbschat, A.; Gretz, N.; Hoffmann, S.C.; Kränzlin, B.; Geiger, H.; Obermüller, N. Kidney Injury Molecule-1 Is Specifically Expressed in Cystically-Transformed Proximal Tubules of the PKD/Mhm (cy/+) Rat Model of Polycystic Kidney Disease. Int. J. Mol. Sci. 2016, 17, 802.

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