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Muscle regeneration, inflammation, and connective tissue expansion in canine inflammatory myopathy
Author(s) -
Salvadori Claudia,
Peters Iain R.,
Day Michael J.,
Engvall Eva,
Shelton G. Diane
Publication year - 2005
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.20252
Subject(s) - pathology , inflammation , fibrosis , connective tissue , regeneration (biology) , myopathy , inflammatory myopathy , chemokine , h&e stain , extracellular matrix , myosin , pathogenesis , myositis , proinflammatory cytokine , medicine , immunohistochemistry , biology , immunology , microbiology and biotechnology
Abstract Inflammatory myopathies (IMs) are relatively common in dogs, and canine IMs have many similarities to human IMs. The aim of this work was to analyze aspects of the pathogenesis of canine IM with an ultimate goal of establishing canine IM as a model for human IM. Muscle biopsies from 16 dogs with a histological diagnosis of IM were analyzed to determine degree of muscle regeneration, presence of eosinophils, expression of selected cytokines and chemokines, and extent of fibrosis. Regeneration, as shown by staining for developmental myosin heavy chain, was more extensive than evidenced with hematoxylin–eosin staining in most cases of canine IM. Expression of mRNA encoding transforming growth factor‐beta (TGF‐β) and eotaxin 3 was upregulated in all cases evaluated. Eosinophils were abundant in most cases, and the connective tissue was variably expanded, as demonstrated by the distribution of the ubiquitous extracellular matrix proteins collagen VI and fibrillin. The extensive regeneration demonstrates that muscle may survive this adverse environment if inflammation and fibrosis can be stopped or reduced. Muscle Nerve, 2005