Myosin loss in denervated rat soleus muscle after dexamethasone treatment

被引：20

作者：

Horinouchi, H ^{[1
]}

Kumamoto, T ^{[1
]}

Kimura, N ^{[1
]}

Ueyama, H ^{[1
]}

Tsuda, T ^{[1
]}

机构：

[1] Oita Univ, Fac Med, Dept Brain & Nerve Sci, Div Neurol & Neuromuscular Disorders, Oita 8795593, Japan

来源：

PATHOBIOLOGY | 2005年 / 72卷 / 03期

关键词：

Atrogin-1; critical illness myopathy; myosin heavy chain; proteasome; ubiquitin-proteasome pathway;

D O I：

10.1159/000084113

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Objective: Critical illness myopathy (CIM) is an acute myopathy that appears in the setting of critical illness or during exposure to corticosteroids and neuromuscular blocking agents. Its pathological feature is selective loss of thick myosin filaments. Our aim is to gain further insight into the pathomechanism of myosin loss in this myopathy. Methods: To clarify the expression of myosin heavy chain (MHC) and ubiquitin ligase atrogin-1 in this myopathy, histological, immunohistochemical, SDS-PAGE, and semiquantitative reverse transcriptase-polymerase chain reaction studies were performed on innervated and denervated rat soleus muscles after saline and dexamethasone treatments. Results: Denervated muscles from dexamethasone-treated rats showed marked MHC loss. The mRNA expression of ubiquitin ligase atrogin-1 was significantly increased in denervated dexamethasone-treated muscles, suggesting that the ubiquitin-proteasome pathway plays an important role in muscular wasting in CIM. Furthermore, mRNA levels of MHC I, a myosin isoform, were decreased in the denervated dexamethasone-treated muscles. Conclusion: Our findings suggest that an altered transcription rate of myosin, as well as the upregulation of multiple ubiquitin ligases, may be responsible for selective myosin loss in this myopathy. Copyright (C) 2005 S. Karger AG, Basel.

引用

页码：108 / 116

页数：9

共 39 条

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