Aquaporin 4 mRNA Levels in Neuromuscular Tissues of Wild-type and Dystrophin-deficient Mice
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- Shibuya Seiji
- Department of Neurology, Showa University Fujigaoka Hospital
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- Hara Hajime
- Department of Neurology, Showa University Fujigaoka Hospital
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- Wakayama Yoshihiro
- Department of Neurology, Showa University Fujigaoka Hospital
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- Inoue Masahiko
- Department of Neurology, Showa University Fujigaoka Hospital
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- Jimi Takahiro
- Department of Neurology, Showa University Fujigaoka Hospital
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- Matsuzaki Yoko
- Biochemical Laboratory, Showa University Fujigaoka Hospital
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Aquaporin (AQP) 4 is a water-specific channel protein and is abundant in central nervous tissues and skeletal muscles. Recently, the AQP4 molecule has been increasingly highlighted in its pathophysiological role of several neurological diseases, such as stroke, muscular dystrophy and neuromyelitis optica. We therefore measured the levels of AQP4 mRNA and glyceraldehyde-3 phosphate dehydrogenase mRNA (an internal control) in muscle and brain tissues of wild-type mice (C57BL10/ScSn) and age-matched dystrophin-deficient mdx mice (C57BL10/ScSn mdx) by real-time quantitative RT-PCR. The relative AQP4 mRNA level was highest in the spinal cord among the neuromuscular tissues examined in wild-type mice. Among the muscle tissues of wild-type mice, the relative AQP4 mRNA level was higher in extensor digitorum longus (EDL) muscles, and its descending order was EDL, quadriceps femoris, soleus and heart muscles. It is noteworthy that there was no difference in the relative AQP4 mRNA levels in the brain tissues between wild-type mice and age-matched mdx mice. In contrast, the AQP4 mRNA level in the quadriceps femoris muscle was significantly lower in mdx mice than in wild-type mice. The fact that the spinal cord contains the highest AQP4 mRNA may be related to the pathogenesis of neuromyelitis optica, in which AQP4 protein is the target antigen. In addition, the low expression level of AQP4 mRNA in the mdx mouse muscle suggests a functional link between AQP4 and dystrophin in the muscle tissue. We suggest that a similar pathomechanism may underlie the phenotypic consequences of the mdx mouse and Duchenne muscular dystrophy.
収録刊行物
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- The Tohoku Journal of Experimental Medicine
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The Tohoku Journal of Experimental Medicine 215 (4), 313-319, 2008
東北ジャーナル刊行会
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詳細情報
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- CRID
- 1390282679217673472
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- NII論文ID
- 130004459705
- 10021951245
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- NII書誌ID
- AA00863920
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- ISSN
- 13493329
- 00408727
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可