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Neuronal NOS is dislocated during muscle atrophy in amyotrophic lateral sclerosis.

Abstract：

:Previously, we demonstrated that neuronal nitric oxide synthase (nNOS) is activated and promotes muscle atrophy in skeletal muscle during tail suspension, a model of unloading and denervation. Here, we examined patients with amyotrophic lateral sclerosis (ALS) and mutant (H46R) SOD1 transgenic (Tg) mice model using immunohistochemistry, Western blotting and real time PCR. We found cytoplasmic nNOS staining of angulated muscle fibers in patients with ALS. We also examined mutant SOD1 Tg mice and found cytoplasmic nNOS staining even before the onset of clinical muscle atrophy. In the Tg mice, nNOS was largely extracted with 100 mM NaCl and barely detected in the pellet fraction, suggesting fragile anchoring of nNOS to the sarcolemma. We also showed an elevated expression of atrogin-1, key molecules in muscle atrophy at the end stage. A common nNOS dislocation/atrogin-1/muscle atrophy pathway among tail suspension, denervation and ALS is suggested. nNOS modulation therapy may be beneficial in several types of muscle atrophy.

journal_name

J Neurol Sci

journal_title

Journal of the neurological sciences

authors

Suzuki N,Mizuno H,Warita H,Takeda S,Itoyama Y,Aoki M

doi

10.1016/j.jns.2010.03.022

subject

Has Abstract

pub_date

2010-07-15 00:00:00

pages

95-101

issue

1-2

eissn

0022-510X

issn

1878-5883

pii

S0022-510X(10)00148-6

journal_volume

294

pub_type

杂志文章

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