Linked Life Data

10797389

Source:http://linkedlifedata.com/resource/pubmed/id/10797389

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2000-5-19
pubmed:abstractText
In this review, the adaptations in myosin heavy chain (MHC) isoform expression induced by chronic reductions in neuromuscular activity (including electrical activation and load bearing) of the intact neuromuscular unit are summarized and evaluated. Several different animal models and human clinical conditions of reduced neuromuscular activity are categorized based on the manner and extent to which they alter the levels of electrical activation and load bearing, resulting in three main categories of reduced activity. These are: 1) reduced activation and load bearing (including spinal cord injury, spinal cord transection, and limb immobilization with the muscle in a shortened position); 2) reduced loading (including spaceflight, hindlimb unloading, bed rest, and unilateral limb unloading); and 3) inactivity (including spinal cord isolation and blockage of motoneuron action potential conduction by tetrodotoxin). All of the models discussed resulted in increased expression of fast MHC isoforms at the protein and/or mRNA levels in slow and fast muscles (with the possible exception of unilateral limb unloading in humans). However, the specific fast MHC isoforms that are induced (usually the MHC-IIx isoform in slow muscle and the MHC-IIb isoform in fast muscle) and the degree and rate of adaptation are dependent upon the animal species and the specific model or condition that is being studied. Recent studies designed to elucidate the mechanisms by which electrical activation and load bearing alter expression of MHC isoforms at the cellular and genetic levels are also reviewed. Two main mechanisms have been proposed, the myogenin:MyoD and calcineurin:NF-AT pathways. Collectively, the data suggest that the regulation of MHC isoform expression involves a complex interaction of multiple control mechanisms including the myogenin:MyoD and calcineurin:NF-AT pathways; however, other intracellular signaling pathways are likely to contribute.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0148-639X
pubmed:author
pubmed:copyrightInfo
Copyright 2000 John Wiley & Sons, Inc.
pubmed:issnType
Print
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
661-79
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Myosin heavy chain isoform expression following reduced neuromuscular activity: potential regulatory mechanisms.
pubmed:affiliation
Department of Human Nutrition, Foods and Exercise, Virginia Polytechnic Institute and State University, Blacksburg, Virginia 24061-0430, USA. bobt@vt.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't