Universität zu Köln

Lehners, Alexander, Lange, Sascha, Niemann, Gianina, Rosendahl, Alva, Meyer-Schwesinger, Catherine, Oh, Jun, Stahl, Rolf, Ehmke, Heimo, Benndorf, Ralf, Klinke, Anna, Baldus, Stephan and Wenzel, Ulrich Otto (2014). Myeloperoxidase deficiency ameliorates progression of chronic kidney disease in mice. Am. J. Physiol.-Renal Physiol., 307 (4). S. F407 - 11. BETHESDA: AMER PHYSIOLOGICAL SOC. ISSN 1522-1466

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Abstract

Myeloperoxidase (MPO) is an enzyme expressed in neutrophils and monocytes/macrophages. Beside its well-defined role in innate immune defence, it may also be responsible for tissue damage. To identify the role of MPO in the progression of chronic kidney disease (CKD), we investigated CKD in a model of renal ablation in MPO knockout and wild-type mice. CKD was induced by 5/6 nephrectomy. Mice were followed for 10 wk to evaluate the impact of MPO deficiency on renal morbidity. Renal ablation induced CKD in wild-type mice with increased plasma levels of MPO compared with controls. No difference was found between MPO-deficient and wild-type mice regarding albuminuria 1 wk after renal ablation, indicating similar acute responses to renal ablation. Over the next 10 wk, however, MPO-deficient mice developed significantly less albuminuria and glomerular injury than wild-type mice. This was accompanied by a significantly lower renal mRNA expression of the fibrosis marker genes plasminogen activator inhibitor-I, collagen type III, and collagen type IV as well as matrix metalloproteinase-2 and matrix metalloproteinase-9. MPO-deficient mice also developed less renal inflammation after renal ablation, as indicated by a lower infiltration of CD3-positive T cells and F4/80-positive monocytes/macrophages compared with wild-type mice. In vitro chemotaxis of monocyte/macrophages isolated from MPO-deficient mice was impaired compared with wild-type mice. No significant differences were observed for mortality and blood pressure after renal ablation. In conclusion, these results demonstrate that MPO deficiency ameliorates renal injury in the renal ablation model of CKD in mice.

Item Type:	Journal Article
Creators:	Creators Email ORCID ORCID Put Code Lehners, Alexander UNSPECIFIED UNSPECIFIED UNSPECIFIED Lange, Sascha UNSPECIFIED UNSPECIFIED UNSPECIFIED Niemann, Gianina UNSPECIFIED UNSPECIFIED UNSPECIFIED Rosendahl, Alva UNSPECIFIED UNSPECIFIED UNSPECIFIED Meyer-Schwesinger, Catherine UNSPECIFIED UNSPECIFIED UNSPECIFIED Oh, Jun UNSPECIFIED UNSPECIFIED UNSPECIFIED Stahl, Rolf UNSPECIFIED UNSPECIFIED UNSPECIFIED Ehmke, Heimo UNSPECIFIED UNSPECIFIED UNSPECIFIED Benndorf, Ralf UNSPECIFIED UNSPECIFIED UNSPECIFIED Klinke, Anna UNSPECIFIED UNSPECIFIED UNSPECIFIED Baldus, Stephan UNSPECIFIED UNSPECIFIED UNSPECIFIED Wenzel, Ulrich Otto UNSPECIFIED UNSPECIFIED UNSPECIFIED
URN:	urn:nbn:de:hbz:38-431938
DOI:	10.1152/ajprenal.00262.2014
Journal or Publication Title:	Am. J. Physiol.-Renal Physiol.
Volume:	307
Number:	4
Page Range:	S. F407 - 11
Date:	2014
Publisher:	AMER PHYSIOLOGICAL SOC
Place of Publication:	BETHESDA
ISSN:	1522-1466
Language:	English
Faculty:	Unspecified
Divisions:	Unspecified
Subjects:	no entry
Uncontrolled Keywords:	Keywords Language HYPOCHLORITE-MODIFIED PROTEINS; RENAL INJURY; EXPERIMENTAL GLOMERULONEPHRITIS; ISCHEMIA-REPERFUSION; ANGIOTENSIN-II; INFLAMMATION; NEUTROPHILS; MECHANISM; APOPTOSIS; HYPERTENSION Multiple languages Physiology; Urology & Nephrology Multiple languages
URI:	http://kups.ub.uni-koeln.de/id/eprint/43193