原创力文档myofiber stress-response in myositis parallel investigations on patients and experimental animal models of muscle regeneration and systemic inflammation肌纤维肌炎并行调查患者的应激反应和肌肉再生和系统性炎症的实验动物模型.pdfVIP
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myofiber stress-response in myositis parallel investigations on patients and experimental animal models of muscle regeneration and systemic inflammation肌纤维肌炎并行调查患者的应激反应和肌肉再生和系统性炎症的实验动物模型
Vitadello et al. Arthritis Research Therapy 2010, 12:R52
/content/12/2/R52
RESEARCH ARTICLE Open Access
Myofiber stress-response in myositis: parallel
investigations on patients and experimental
animal models of muscle regeneration and
systemic inflammation
1† 2† 2,3 2 3*
Maurizio Vitadello , Andrea Doria , Elena Tarricone , Anna Ghirardello , Luisa Gorza
Abstract
Introduction: The endoplasmic reticulum (ER) stress-response, evoked in mice by the overexpression of class I
major histocompatibility complex antigen (MHC-I), was proposed as a major mechanism responsible for skeletal
muscle damage and dysfunction in autoimmune myositis. The present study was undertaken to characterize in
more detail the ER stress-response occurring in myofibers of patients with inflammatory myopathies, focusing on
the expression and distribution of Grp94, calreticulin and Grp75, three ER chaperones involved in
immunomodulation.
Methods: Muscle biopsies were obtained from seven healthy subjects and 29 myositis patients, who were
subdivided into groups based on the morphological evidence of inflammation and/or sarcolemmal
immunoreactivity for MHC-I. Biopsies were analyzed by means of immunohistochemistry and western blot using
anti-Grp94, anti-calreticulin and anti-Grp75 specific antibodies. Parallel analyses on these ER chaperones were
conducted in rabbit and/or murine skeletal muscle after experimental induction of regeneration or systemic
inflammation.
Results: Upregulation of Grp94 characterized regenerating myofibers of myositis patients (P = 0.03, compared with
values detected in biopsies without signs of muscle regeneration) and developing and regenerating myofibers of
mouse muscles. Conversely, levels of calreticulin
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