open access

Vol 55, No 2 (2017)
Original paper
Submitted: 2017-03-21
Accepted: 2017-06-07
Published online: 2017-06-12
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Cardiomyocyte marker expression in dogs with left atrial enlargement due to dilated cardiomyopathy or myxomatous mitral valve disease

Izabela Janus1, Malgorzata Kandefer-Gola, Rafal Ciaputa, Agnieszka Noszczyk-Nowak, Urszula Paslawska, Massimiliano Tursi, Marcin Nowak
·
Pubmed: 28612341
·
Folia Histochem Cytobiol 2017;55(2):52-61.
Affiliations
  1. Division of Pathomorphology and Veterinary Forensics, Department of Pathology, Wroclaw University of Environmental and Life Sciences, Wroclaw, Poland, Poland

open access

Vol 55, No 2 (2017)
ORIGINAL PAPERS
Submitted: 2017-03-21
Accepted: 2017-06-07
Published online: 2017-06-12

Abstract

Introduction. Dilated cardiomyopathy (DCM) and myxomatous mitral valve disease (MMVD) are common heart conditions in dogs. They have different etiology and pathogenesis and although other studies focused on changes in the left ventricles of the affected hearts, the aim of our study was to assess the expressions of some intrinsic proteins in the enlarged left atria.

Material and methods. We performed an immunohistochemical analysis of left atrial specimens obtained from 15 dogs with DCM, 35 dogs with MMVD and six control dogs. We assessed the expression of following proteins: SERCA1, SERCA2, sarcomeric actinin, smooth muscle actin, and dystrophin.

Results. We noted a higher percentage of SERCA1-positive cells in the MMVD group and lower percentage of dystrophin-positive cells in the DCM group as compared to control group. The expression of other proteins was similar in the hearts of control dogs and dogs with heart diseases.

Conclusions. The observed changes in the expression patterns of some proteins in the atria of dogs with DCM and MMVD suggest that atrial enlargement relies not only on volume overload, but also alterations of the intrinsic proteins can contribute to the pathogenesis of dilated cardiomyopathy.  

Abstract

Introduction. Dilated cardiomyopathy (DCM) and myxomatous mitral valve disease (MMVD) are common heart conditions in dogs. They have different etiology and pathogenesis and although other studies focused on changes in the left ventricles of the affected hearts, the aim of our study was to assess the expressions of some intrinsic proteins in the enlarged left atria.

Material and methods. We performed an immunohistochemical analysis of left atrial specimens obtained from 15 dogs with DCM, 35 dogs with MMVD and six control dogs. We assessed the expression of following proteins: SERCA1, SERCA2, sarcomeric actinin, smooth muscle actin, and dystrophin.

Results. We noted a higher percentage of SERCA1-positive cells in the MMVD group and lower percentage of dystrophin-positive cells in the DCM group as compared to control group. The expression of other proteins was similar in the hearts of control dogs and dogs with heart diseases.

Conclusions. The observed changes in the expression patterns of some proteins in the atria of dogs with DCM and MMVD suggest that atrial enlargement relies not only on volume overload, but also alterations of the intrinsic proteins can contribute to the pathogenesis of dilated cardiomyopathy.  

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Keywords

dog; heart failure; dilated cardiomyopathy; myxomatous mitral valve disease; left atrium; dystrophin; SERCA1; IHC

About this article
Title

Cardiomyocyte marker expression in dogs with left atrial enlargement due to dilated cardiomyopathy or myxomatous mitral valve disease

Journal

Folia Histochemica et Cytobiologica

Issue

Vol 55, No 2 (2017)

Article type

Original paper

Pages

52-61

Published online

2017-06-12

Page views

1889

Article views/downloads

1833

DOI

10.5603/FHC.a2017.0009

Pubmed

28612341

Bibliographic record

Folia Histochem Cytobiol 2017;55(2):52-61.

Keywords

dog
heart failure
dilated cardiomyopathy
myxomatous mitral valve disease
left atrium
dystrophin
SERCA1
IHC

Authors

Izabela Janus
Malgorzata Kandefer-Gola
Rafal Ciaputa
Agnieszka Noszczyk-Nowak
Urszula Paslawska
Massimiliano Tursi
Marcin Nowak

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