open access

Vol 51, No 1 (2013)
Original paper
Submitted: 2013-04-28
Accepted: 2013-04-28
Published online: 2013-04-24
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CCN1 expression in interleukin-6 deficient mouse kidney in experimental model of heart failure

Tomasz Andrzej Bonda, Andrzej Taranta, Karol Adam Kaminski, Magdalena Dziemidowicz, Sergey Litvinovich, Marcin Kozuch, Izabela Bialuk, Lech Chyczewski, Maria Malgorzata Winnicka
DOI: 10.5603/FHC.2013.0012
·
Folia Histochem Cytobiol 2013;51(1):84-91.

open access

Vol 51, No 1 (2013)
ORIGINAL PAPERS
Submitted: 2013-04-28
Accepted: 2013-04-28
Published online: 2013-04-24

Abstract

Chronic heart failure often leads to worsening of the renal function. Mediators of this process include inflammatory and neuroendocrine factors. CCN1 (Cyr 61), a member of growth factor-inducible immediate early genes, which modulates inflammation and fibrogenesis, is excreted with urine in the early phase of acute renal injury and may be involved in the pathogenesis of the cardiorenal syndrome. The aim of the study was to evaluate CCN1 protein abundance and localization in the kidney of IL-6-deficient C57BL/6J (IL-6 KO) mice and respective wild-type (WT) animals in basal conditions and in animals with chronic heart failure twelve weeks after myocardial infarction. Age- and sex-matched mice from both strains subjected to sham operation served as controls. One group of WT animals subjected to myocardial infarction was treated with antagonist of AT1 receptor telmisartan over 12 weeks. Abundance and localization of CCN1 protein in kidney were assessed with Western blotting and immunohistochemistry, respectively. In all groups the strongest immunohistochemical reaction for CCN1 was observed in distal convoluted tubules and in smaller arteries, however, the total expression of CCN1 protein was lower in IL-6 KO mice in comparison to WT animals. The main difference in CCN1 distribution between the examined genotypes was lack of reaction in internal renal medulla and very weak reaction in proximal convoluted tubules in IL-6 KO mice. Experimental heart failure only slightly attenuated the expression of CCN1 protein in the kidney of WT mice and had no effect in IL-6 KO mice. Although, blockade of AT1 receptor did not alter CCN1 protein expression in kidneys of WT mice after myocardial infarction, it significantly changed its CCN1 distribution in the renal tubular system. (Folia Histochemica et Cytobiologica 2013, Vol. 51, No. 1, 84–91)

Abstract

Chronic heart failure often leads to worsening of the renal function. Mediators of this process include inflammatory and neuroendocrine factors. CCN1 (Cyr 61), a member of growth factor-inducible immediate early genes, which modulates inflammation and fibrogenesis, is excreted with urine in the early phase of acute renal injury and may be involved in the pathogenesis of the cardiorenal syndrome. The aim of the study was to evaluate CCN1 protein abundance and localization in the kidney of IL-6-deficient C57BL/6J (IL-6 KO) mice and respective wild-type (WT) animals in basal conditions and in animals with chronic heart failure twelve weeks after myocardial infarction. Age- and sex-matched mice from both strains subjected to sham operation served as controls. One group of WT animals subjected to myocardial infarction was treated with antagonist of AT1 receptor telmisartan over 12 weeks. Abundance and localization of CCN1 protein in kidney were assessed with Western blotting and immunohistochemistry, respectively. In all groups the strongest immunohistochemical reaction for CCN1 was observed in distal convoluted tubules and in smaller arteries, however, the total expression of CCN1 protein was lower in IL-6 KO mice in comparison to WT animals. The main difference in CCN1 distribution between the examined genotypes was lack of reaction in internal renal medulla and very weak reaction in proximal convoluted tubules in IL-6 KO mice. Experimental heart failure only slightly attenuated the expression of CCN1 protein in the kidney of WT mice and had no effect in IL-6 KO mice. Although, blockade of AT1 receptor did not alter CCN1 protein expression in kidneys of WT mice after myocardial infarction, it significantly changed its CCN1 distribution in the renal tubular system. (Folia Histochemica et Cytobiologica 2013, Vol. 51, No. 1, 84–91)

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Keywords

CCN1; kidney; heart failure; IL-6 deficient mice; telmisartan

About this article
Title

CCN1 expression in interleukin-6 deficient mouse kidney in experimental model of heart failure

Journal

Folia Histochemica et Cytobiologica

Issue

Vol 51, No 1 (2013)

Article type

Original paper

Pages

84-91

Published online

2013-04-24

DOI

10.5603/FHC.2013.0012

Bibliographic record

Folia Histochem Cytobiol 2013;51(1):84-91.

Keywords

CCN1
kidney
heart failure
IL-6 deficient mice
telmisartan

Authors

Tomasz Andrzej Bonda
Andrzej Taranta
Karol Adam Kaminski
Magdalena Dziemidowicz
Sergey Litvinovich
Marcin Kozuch
Izabela Bialuk
Lech Chyczewski
Maria Malgorzata Winnicka

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